bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2021–10–24
38 papers selected by
Ayesh Seneviratne, University of Toronto



  1. Int J Mol Sci. 2021 Oct 15. pii: 11117. [Epub ahead of print]22(20):
      Mitochondrial dysfunction and stem cell exhaustion are two hallmarks of aging. In the hematopoietic system, aging is linked to imbalanced immune response and reduced regenerative capacity in hematopoietic stem cells (HSCs), as well as an increased predisposition to a spectrum of diseases, including myelodysplastic syndrome and acute myeloid leukemia. Myeloid-biased differentiation and loss of polarity are distinct features of aged HSCs, which generally exhibit enhanced mitochondrial oxidative phosphorylation and increased production of reactive oxygen species (ROS), suggesting a direct role for mitochondria in the degenerative process. Here, we provide an overview of current knowledge of the mitochondrial mechanisms that contribute to age-related phenotypes in HSCs. These include mitochondrial ROS production, alteration/activation of mitochondrial metabolism, the quality control pathway of mitochondria, and inflammation. Greater understanding of the key machineries of HSC aging will allow us to identify new therapeutic targets for preventing, delaying, or even reversing aspects of this process.
    Keywords:  ROS; aging; hematopoiesis; hematopoietic stem cell; inflammation; mitochondrial metabolism; stem cell exhaustion
    DOI:  https://doi.org/10.3390/ijms222011117
  2. Blood Cancer Discov. 2021 May;2(3): 192-194
      The study of clonal hematopoiesis is rapidly evolving, with the highest prevalence in aging populations and wide-ranging implications for health and disease, including an increased risk of subsequent myeloid malignancies and cardiovascular disease. In their article, Feusier and colleagues report on an expanded driver mutation list for capture of higher-risk clonal hematopoiesis mutations implicated in leukemia transformation. They also describe the prevalence of clonal hematopoiesis in several additional large studies, including, most importantly, in the pediatric context, which has not yet been extensively studied with respect to clonal hematopoiesis and clonal hematopoiesis-related sequelae. See related article by Feusier et al., p. 226.
    DOI:  https://doi.org/10.1158/2643-3230.BCD-21-0025
  3. Cells. 2021 Oct 16. pii: 2775. [Epub ahead of print]10(10):
      Mitochondria are ubiquitous organelles of eukaryotic organisms with a number of essential functions, including synthesis of iron-sulfur clusters, amino acids, lipids, and adenosine triphosphate (ATP). During aging of the fungal aging model Podospora anserina, the inner mitochondrial membrane (IMM) undergoes prominent morphological alterations, ultimately resulting in functional impairments. Since phospholipids (PLs) are key components of biological membranes, maintenance of membrane plasticity and integrity via regulation of PL biosynthesis is indispensable. Here, we report results from a lipidomic analysis of isolated mitochondria from P. anserina that revealed an age-related reorganization of the mitochondrial PL profile and the involvement of the i-AAA protease PaIAP in proteolytic regulation of PL metabolism. The absence of PaIAP enhances biosynthesis of characteristic mitochondrial PLs, leads to significant alterations in the acyl composition of the mitochondrial signature PL cardiolipin (CL), and induces mitophagy. These alterations presumably cause the lifespan increase of the PaIap deletion mutant under standard growth conditions. However, PaIAP is required at elevated temperatures and for degradation of superfluous CL synthase PaCRD1 during glycolytic growth. Overall, our study uncovers a prominent role of PaIAP in the regulation of PL homeostasis in order to adapt membrane plasticity to fluctuating environmental conditions as they occur in nature.
    Keywords:  P. anserina; PaCRD1; PaIAP; aging; lipid metabolism; mitochondria
    DOI:  https://doi.org/10.3390/cells10102775
  4. Front Nutr. 2021 ;8 758058
      The average human life expectancy continues to rise globally and so does the prevalence and absolute burden of cardiovascular disease. Dietary restriction promotes longevity and improves various cardiovascular risk factors, including hypertension, obesity, diabetes mellitus, and metabolic syndrome. However, low adherence to caloric restriction renders this stringent dietary intervention challenging to adopt as a standard practice for cardiovascular disease prevention. Hence, alternative eating patterns and strategies that recapitulate the salutary benefits of caloric restriction are under intense investigation. Here, we first provide an overview of alternative interventions, including intermittent fasting, alternate-day fasting and the Mediterranean diet, along with their cardiometabolic effects in animal models and humans. We then present emerging pharmacological alternatives, including spermidine, NAD+ precursors, resveratrol, and metformin, as promising caloric restriction mimetics, and briefly touch on the mechanisms underpinning their cardiometabolic and health-promoting effects. We conclude that implementation of feasible dietary approaches holds the promise to attenuate the burden of cardiovascular disease and facilitate healthy aging in humans.
    Keywords:  autophagy; caloric restriction; caloric restriction mimetics; cardiovascular risk factors; dietary regimens; hypertension; intermittent fasting; obesity
    DOI:  https://doi.org/10.3389/fnut.2021.758058
  5. Cell Stem Cell. 2021 Oct 13. pii: S1934-5909(21)00390-8. [Epub ahead of print]
      N6-methyladenosine (m6A) on mRNA plays critical roles in various cellular processes. However, the landscape and dynamics of m6A modification in hematopoietic system remain unknown. Here, we delineate a comprehensive m6A landscape across hematopoietic hierarchy and uncover that IGF2BP2 is required for preserving the function of hematopoietic stem cells (HSCs). Our data reveal a cell-type-specific m6A landscape in hematopoiesis. m6A modifications arise mostly in the early stage of hematopoiesis and prefer to play distinct roles for determining mRNA fates in HSCs and committed progenitors. Mechanistically, increased m6A-IGF2BP2 expression controls transcriptional state and maintenance of HSCs. IGF2BP2 deficiency induces quiescence loss and impairs HSC function. Moreover, IGF2BP2 loss increases mitochondrial activity of HSCs by accelerating Bmi1 mRNA decay, leading to de-repression of mitochondria-related genes. Collectively, our results present a fascinating portrait of m6A modification of hematopoietic hierarchy and reveal a key role of IGF2BP2 in maintaining HSC function by restraining mitochondrial activity.
    Keywords:  IGF2BP2; N6-methyladenosine; hematopoiesis; hematopoietic stem cells
    DOI:  https://doi.org/10.1016/j.stem.2021.09.014
  6. Cells. 2021 Oct 13. pii: 2729. [Epub ahead of print]10(10):
      In recent years, aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered to be involved in aging phenotypes across several species. This receptor is a highly conserved biosensor that is activated by numerous exogenous and endogenous molecules, including microbiota metabolites, to mediate several physiological and toxicological functions. Brain aging hallmarks, which include glial cell activation and inflammation, increased oxidative stress, mitochondrial dysfunction, and cellular senescence, increase the vulnerability of humans to various neurodegenerative diseases. Interestingly, many studies have implicated AhR signaling pathways in the aging process and longevity across several species. This review provides an overview of the impact of AhR pathways on various aging hallmarks in the brain and the implications for AhR signaling as a mechanism in regulating aging-related diseases of the brain. We also explore how the nature of AhR ligands determines the outcomes of several signaling pathways in brain aging processes.
    Keywords:  AhR endogenous/exogenous ligands; aryl hydrocarbon receptor; brain aging hallmarks; neurodegenerative diseases
    DOI:  https://doi.org/10.3390/cells10102729
  7. Nat Metab. 2021 Oct;3(10): 1327-1341
      Calorie restriction (CR) promotes healthy ageing in diverse species. Recently, it has been shown that fasting for a portion of each day has metabolic benefits and promotes lifespan. These findings complicate the interpretation of rodent CR studies, in which animals typically eat only once per day and rapidly consume their food, which collaterally imposes fasting. Here we show that a prolonged fast is necessary for key metabolic, molecular and geroprotective effects of a CR diet. Using a series of feeding regimens, we dissect the effects of calories and fasting, and proceed to demonstrate that fasting alone recapitulates many of the physiological and molecular effects of CR. Our results shed new light on how both when and how much we eat regulate metabolic health and longevity, and demonstrate that daily prolonged fasting, and not solely reduced caloric intake, is likely responsible for the metabolic and geroprotective benefits of a CR diet.
    DOI:  https://doi.org/10.1038/s42255-021-00466-9
  8. J Pers Med. 2021 Oct 18. pii: 1043. [Epub ahead of print]11(10):
      The progressive loss of the regenerative potential of tissues is one of the most obvious consequences of aging, driven by altered intercellular communication, cell senescence and niche-specific stem cell exhaustion, among other drivers. Mesenchymal tissues, such as bone, cartilage and fat, which originate from mesenchymal stem cell (MSC) differentiation, are especially affected by aging. Senescent MSCs show limited proliferative capacity and impairment in key defining features: their multipotent differentiation and secretory abilities, leading to diminished function and deleterious consequences for tissue homeostasis. In the past few years, several interventions to improve human healthspan by counteracting the cellular and molecular consequences of aging have moved closer to the clinic. Taking into account the MSC exhaustion occurring in aging, advanced therapies based on the potential use of young allogeneic MSCs and derivatives, such as extracellular vesicles (EVs), are gaining attention. Based on encouraging pre-clinical and clinical data, this review assesses the strong potential of MSC-based (cell and cell-free) therapies to counteract age-related consequences in both physiological and premature aging scenarios. We also discuss the mechanisms of action of these therapies and the possibility of enhancing their clinical potential by exposing MSCs to niche-relevant signals.
    Keywords:  MSCs; cell therapies; cell-free therapies; extracellular vesicles; inflammation; paracrine mechanism; physiological aging; premature aging; stem cell exhaustion
    DOI:  https://doi.org/10.3390/jpm11101043
  9. Mech Ageing Dev. 2021 Oct 18. pii: S0047-6374(21)00156-1. [Epub ahead of print] 111584
      Understanding the molecular mechanisms of normal aging is a prerequisite to significantly improving human health span. Caloric restriction (CR) can delay aging and has served as a yardstick to evaluate interventions extending life span. However, mice given unlimited access to food suffer severe obesity. Health gains from CR depend on control mice being sufficiently overweight and less obese mouse strains benefit far less from CR. Pharmacologic interventions that increase life span, including resveratrol, rapamycin, nicotinamide mononucleotide and metformin, also reduce body weight. In primates, CR does not delay aging unless the control group is eating enough to suffer from obesity-related disease. Human survival is optimal at a body mass index achievable without CR, and the above interventions are merely diet aids that shouldn't slow aging in healthy weight individuals.CR in humans of optimal weight can safely be declared useless, since there is overwhelming evidence that hunger, underweight and starvation reduce fitness, survival, and quality of life. Against an obese control, CR does, however, truly delay aging through a mechanism laid out in the following tumor suppression theory of aging.
    Keywords:  Aging; Caloric restriction; Caloric restriction mimetics; Life span; Obesity
    DOI:  https://doi.org/10.1016/j.mad.2021.111584
  10. Nat Rev Mol Cell Biol. 2021 Oct 18.
      Skeletal muscle contains a designated population of adult stem cells, called satellite cells, which are generally quiescent. In homeostasis, satellite cells proliferate only sporadically and usually by asymmetric cell division to replace myofibres damaged by daily activity and maintain the stem cell pool. However, satellite cells can also be robustly activated upon tissue injury, after which they undergo symmetric divisions to generate new stem cells and numerous proliferating myoblasts that later differentiate to muscle cells (myocytes) to rebuild the muscle fibre, thereby supporting skeletal muscle regeneration. Recent discoveries show that satellite cells have a great degree of population heterogeneity, and that their cell fate choices during the regeneration process are dictated by both intrinsic and extrinsic mechanisms. Extrinsic cues come largely from communication with the numerous distinct stromal cell types in their niche, creating a dynamically interactive microenvironment. This Review discusses the role and regulation of satellite cells in skeletal muscle homeostasis and regeneration. In particular, we highlight the cell-intrinsic control of quiescence versus activation, the importance of satellite cell-niche communication, and deregulation of these mechanisms associated with ageing. The increasing understanding of how satellite cells are regulated will help to advance muscle regeneration and rejuvenation therapies.
    DOI:  https://doi.org/10.1038/s41580-021-00421-2
  11. Nat Metab. 2021 Oct;3(10): 1290-1301
      Cellular senescence entails a permanent proliferative arrest, coupled to multiple phenotypic changes. Among these changes is the release of numerous biologically active molecules collectively known as the senescence-associated secretory phenotype, or SASP. A growing body of literature indicates that both senescence and the SASP are sensitive to cellular and organismal metabolic states, which in turn can drive phenotypes associated with metabolic dysfunction. Here, we review the current literature linking senescence and metabolism, with an eye toward findings at the cellular level, including both metabolic inducers of senescence and alterations in cellular metabolism associated with senescence. Additionally, we consider how interventions that target either metabolism or senescent cells might influence each other and mitigate some of the pro-aging effects of cellular senescence. We conclude that the most effective interventions will likely break a degenerative feedback cycle by which cellular senescence promotes metabolic diseases, which in turn promote senescence.
    DOI:  https://doi.org/10.1038/s42255-021-00483-8
  12. Nat Med. 2021 Oct 18.
      Clonal hematopoiesis (CH) results from somatic genomic alterations that drive clonal expansion of blood cells. Somatic gene mutations associated with hematologic malignancies detected in hematopoietic cells of healthy individuals, referred to as CH of indeterminate potential (CHIP), have been associated with myeloid malignancies, while mosaic chromosomal alterations (mCAs) have been associated with lymphoid malignancies. Here, we analyzed CHIP in 55,383 individuals and autosomal mCAs in 420,969 individuals with no history of hematologic malignancies in the UK Biobank and Mass General Brigham Biobank. We distinguished myeloid and lymphoid somatic gene mutations, as well as myeloid and lymphoid mCAs, and found both to be associated with risk of lineage-specific hematologic malignancies. Further, we performed an integrated analysis of somatic alterations with peripheral blood count parameters to stratify the risk of incident myeloid and lymphoid malignancies. These genetic alterations can be readily detected in clinical sequencing panels and used with blood count parameters to identify individuals at high risk of developing hematologic malignancies.
    DOI:  https://doi.org/10.1038/s41591-021-01521-4
  13. Cell Chem Biol. 2021 Oct 21. pii: S2451-9456(21)00435-9. [Epub ahead of print]28(10): 1390-1392
      Sumoylation is a reversible post-translational modification implicated in cancer. In this issue of Cell Chemical Biology, Benoit et al. describe an inhibitor of sumoylation that results in anti-proliferative effects in cancer stem cell models via the sumoylation enzyme SAE2.
    DOI:  https://doi.org/10.1016/j.chembiol.2021.10.001
  14. World J Urol. 2021 Oct 17.
       PURPOSE OF REVIEW: A sound scientific basis has been emerging on the anti-neoplastic role of metformin, statins and dietary interventions. However, evidence in prostate cancer patients remains mixed owing to an absence of completed randomized trials. This overview examines the rationale for metformin, statins and dietary intervention for secondary prevention in men on active surveillance by summarizing current evidence base and biological mechanisms in influencing cancer progression and mortality.
    METHODS: A comprehensive literature search was performed to identify studies that evaluated the role of metformin, statins and diet in the secondary prevention of prostate cancer as well as those that described the anti-cancer mechanisms of these agents. The search included Pubmed, MEDLINE, EMBASE and Cochrane library from inception till August 2021.
    RESULTS: A total of 14 trials on metformin, 21 trials on statins and 13 trials on dietary measures were evaluated. Majority were observational population-based cohort studies or meta-analysis of them. Three ongoing prospective randomized controlled trials were also reported. Overall, mixed results were obtained.
    CONCLUSIONS: The role of metformin and statins remains promising with several trials showing reduced rates of progression and cancer specific mortality. Combination therapy strategies have also been evaluated in more advanced patients showing synergism. Dietary interventions especially fruits, vegetables and fish intake has shown some benefit albeit with mixed results for others like legumes, red meat, coffee and multivitamins. Several ongoing randomized trials will provide stronger evidence in the future for secondary prevention.
    Keywords:  Active surveillance; Diet; Metformin; Prostate cancer; Statins
    DOI:  https://doi.org/10.1007/s00345-021-03858-4
  15. Cells. 2021 Sep 27. pii: 2549. [Epub ahead of print]10(10):
      Iron metabolism and heme biosynthesis are essential processes in cells during the energy cycle. Alteration in these processes could create an inflammatory condition, which results in tumorigenesis. Studies are conducted on the exact role of iron/heme metabolism in induced inflammatory conditions. This study used lipopolysaccharide (LPS)- or high-glucose-induced inflammation conditions in THP-1 cells to study how iron/heme metabolism participates in inflammatory responses. Here, we used iron and heme assays for measuring total iron and heme. We also used flow cytometry and Western blotting to analyze molecular responses. Our results demonstrated that adding LPS or high-glucose induced iron formation and heme synthesis and elevated the expression levels of proteins responsible for iron metabolism and heme synthesis. We then found that further addition of heme or 5-aminolevulinic acid (ALA) increased heme biosynthesis and promoted inflammatory responses by upregulating TLR4/NF-κB and inflammatory cytokine expressions. We also demonstrated the inhibition of heme synthesis using succinylacetone (SA). Moreover, N-MMP inhibited LPS- or high-glucose-induced inflammatory responses by inhibiting TLR4/NF-κB signaling. Hence, iron/heme metabolism checkpoints could be considered a target for treating inflammatory conditions.
    Keywords:  LPS; TLR4/NF-κB; heme biosynthesis; high glucose; inflammatory response; iron metabolism
    DOI:  https://doi.org/10.3390/cells10102549
  16. Metabolites. 2021 Oct 15. pii: 705. [Epub ahead of print]11(10):
      I'm Not Dead Yet (Indy) is a fly gene that encodes a homologue of mammalian SLC13A5 plasma membrane citrate transporter. Reducing expression of Indy gene in flies, and its homologues in worms, extends longevity. Indy reduction in flies, worms, mice and rats affects metabolism by regulating the levels of cytoplasmic citrate, inducing a state similar to calorie restriction. Changes include lower lipid levels, increased insulin sensitivity, increased mitochondrial biogenesis, and prevention of weight gain, among others. The INDY protein is predominantly expressed in fly metabolic tissues: the midgut, fat body and oenocytes. Changes in fly midgut metabolism associated with reduced Indy gene activity lead to preserved mitochondrial function and reduced production of reactive oxygen species. All these changes lead to preserved intestinal stem cell homeostasis, which has a key role in maintaining intestinal epithelium function and enhancing fly healthspan and lifespan. Indy gene expression levels change in response to caloric content of the diet, inflammation and aging, suggesting that INDY regulates metabolic adaptation to nutrition or energetic requirements by controlling citrate levels.
    Keywords:  Indy; SLC13A5; aging; citrate transporter; intestinal stem cells; longevity gene; metabolism
    DOI:  https://doi.org/10.3390/metabo11100705
  17. Cells. 2021 Sep 22. pii: 2507. [Epub ahead of print]10(10):
      Sphingolipids, associated enzymes, and the sphingolipid pathway are implicated in complex, multifaceted roles impacting several cell functions, such as cellular homeostasis, apoptosis, cell differentiation, and more through intrinsic and autocrine/paracrine mechanisms. Given this broad range of functions, it comes as no surprise that a large body of evidence points to important functions of sphingolipids in hematopoiesis. As the understanding of the processes that regulate hematopoiesis and of the specific characteristics that define each type of hematopoietic cells is being continuously refined, the understanding of the roles of sphingolipid metabolism in hematopoietic lineage commitment is also evolving. Recent findings indicate that sphingolipid alterations can modulate lineage commitment from stem cells all the way to megakaryocytic, erythroid, myeloid, and lymphoid cells. For instance, recent evidence points to the ability of de novo sphingolipids to regulate the stemness of hematopoietic stem cells while a substantial body of literature implicates various sphingolipids in specialized terminal differentiation, such as thrombopoiesis. This review provides a comprehensive discussion focused on the mechanisms that link sphingolipids to the commitment of hematopoietic cells to the different lineages, also highlighting yet to be resolved questions.
    Keywords:  ceramide; erythrocytes; hematopoiesis; hematopoietic stem cells; lineage commitment; lymphoid differentiation; megakaryocytes; myeloid differentiation; sphingolipids; sphingosine-1-phosphate
    DOI:  https://doi.org/10.3390/cells10102507
  18. Int J Environ Res Public Health. 2021 Oct 12. pii: 10666. [Epub ahead of print]18(20):
      Impairment of vascular function, in particular endothelial dysfunction and large elastic artery stiffening, represents a major link between ageing and cardiovascular risk. Clinical and experimental studies identified numerous mechanisms responsible for age-related decline of endothelial function and arterial compliance. Since most of these mechanisms are related to oxidative stress or low-grade inflammation, strategies that suppress oxidative stress and inflammation could be effective for preventing age-related changes in arterial function. Indeed, aerobic physical activity, which has been shown to improve intracellular redox balance and mitochondrial health and reduce levels of systemic inflammatory markers, also improves endothelial function and arterial distensibility and reduces risk of cardiovascular diseases. The present paper provides a brief overview of processes underlying age-related changes in arterial function, as well as the mechanisms through which aerobic exercise might prevent or interrupt these processes, and thus attenuate vascular ageing.
    Keywords:  aerobic exercise; ageing; arterial stiffness; endothelial dysfunction
    DOI:  https://doi.org/10.3390/ijerph182010666
  19. Int J Environ Res Public Health. 2021 Oct 19. pii: 10974. [Epub ahead of print]18(20):
      It has been considered that widowed persons have a higher risk of death. This study intended to explore whether social participation could improve this trend. A longitudinal study database was constructed to explore the trend of survival and its change with social participation in widowed persons. The Taiwan Longitudinal Study on Aging (TLSA), based on four consecutive waves of longitudinal follow-up data in 1999, 2003, 2007, and 2011 was linked with the National Death Registry from 1999 through 2012. In total, there were 1417 widowed persons and 4500 nonwidowed persons included in this study, excluding divorced and never-married people. The survival trend analysis was carried out with social participation as the main predictive factor stratified for comparative analysis. Our results showed that the widowed were older than the nonwidowed, were female-dominant, had a lower education level, were more economically stressed, and were less likely to engage in regular exercise, and thus showed generally poorer health; for example, being more vulnerable to having chronic diseases, disability with the Activities of Daily Living (ADL), cognitive impairment with the Short Portable Mental State Questionnaire (SPMSQ), and depression with The Center for Epidemiological Studies-Depression (CES-D). The death risk of the widowed was significantly higher than that of the nonwidowed, but the death trend for those with social participation was significantly lower than that of their counterparts in both the widowed and nonwidowed. After matching with gender and age for widowed persons, the widowed with social participation had a significantly lower risk of death (adjusted hazard ratio (HR), 0.83; 95% confidence interval (CI), 0.71-0.98) compared to the widowed without social participation. It was concluded that social participation can improve the death risk for the widowed, and it is worthily included in health promotion plans and social welfare services for widowed persons.
    Keywords:  mortality; social participation; survival; widowed persons
    DOI:  https://doi.org/10.3390/ijerph182010974
  20. FEBS J. 2021 Oct 22.
      Within the growing field of amino acid metabolism, tryptophan (Trp) catabolism is an area of increasing interest. Trp is essential for protein synthesis, and its metabolism gives rise to biologically active catabolites including serotonin and numerous metabolites in the kynurenine (Kyn) pathway. In normal tissues, the production of Trp metabolites is directly regulated by the tissue-specific expression of Trp-metabolizing enzymes. Alterations of these enzymes in cancers can shift the balance and lead to an increased production of specific byproducts that can function as oncometabolites. For example, increased expression of the enzyme IDO1, which converts Trp into Kyn, leads to an increase in Kyn levels in numerous cancers. Kyn functions as an oncometabolite in cancer cells by promoting the activity of the transcription factor aryl hydrocarbon receptor (AHR), which regulates pro-growth genes. Moreover, Kyn also inhibits T cell activity and thus allows cancer cells to evade clearance by the immune system. Therefore, targeting the Kyn pathway has become a therapeutic focus as a novel means to abrogate tumor growth and immune resistance. This review summarizes the biological role and regulation of Trp metabolism and its catabolites with an emphasis on tumor cell growth and immune evasion, and outlines areas for future research focus.
    Keywords:  AHR; IDO1; TDO2; cancer; immune evasion; kynurenine; proliferation; tryptophan
    DOI:  https://doi.org/10.1111/febs.16245
  21. Cochrane Database Syst Rev. 2021 Oct 18. 10 CD015045
       BACKGROUND: The development of severe coronavirus disease 2019 (COVID-19) and poor clinical outcomes are associated with hyperinflammation and a complex dysregulation of the immune response. Colchicine is an anti-inflammatory medicine and is thought to improve disease outcomes in COVID-19 through a wide range of anti-inflammatory mechanisms. Patients and healthcare systems need more and better treatment options for COVID-19 and a thorough understanding of the current body of evidence.
    OBJECTIVES: To assess the effectiveness and safety of Colchicine as a treatment option for COVID-19 in comparison to an active comparator, placebo, or standard care alone in any setting, and to maintain the currency of the evidence, using a living systematic review approach.
    SEARCH METHODS: We searched the Cochrane COVID-19 Study Register (comprising CENTRAL, MEDLINE (PubMed), Embase, ClinicalTrials.gov, WHO International Clinical Trials Registry Platform, and medRxiv), Web of Science (Science Citation Index Expanded and Emerging Sources Citation Index), and WHO COVID-19 Global literature on coronavirus disease to identify completed and ongoing studies without language restrictions to 21 May 2021.
    SELECTION CRITERIA: We included randomised controlled trials evaluating colchicine for the treatment of people with COVID-19, irrespective of disease severity, age, sex, or ethnicity. We excluded studies investigating the prophylactic effects of colchicine for people without severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection but at high risk of SARS-CoV-2 exposure.
    DATA COLLECTION AND ANALYSIS: We followed standard Cochrane methodology. We used the Cochrane risk of bias tool (ROB 2) to assess bias in included studies and GRADE to rate the certainty of evidence for the following prioritised outcome categories considering people with moderate or severe COVID-19: all-cause mortality, worsening and improvement of clinical status, quality of life, adverse events, and serious adverse events and for people with asymptomatic infection or mild disease: all-cause mortality, admission to hospital or death, symptom resolution, duration to symptom resolution, quality of life, adverse events, serious adverse events.
    MAIN RESULTS: We included three RCTs with 11,525 hospitalised participants (8002 male) and one RCT with 4488 (2067 male) non-hospitalised participants. Mean age of people treated in hospital was about 64 years, and was 55 years in the study with non-hospitalised participants. Further, we identified 17 ongoing studies and 11 studies completed or terminated, but without published results. Colchicine plus standard care versus standard care (plus/minus placebo) Treatment of hospitalised people with moderate to severe COVID-19 All-cause mortality: colchicine plus standard care probably results in little to no difference in all-cause mortality up to 28 days compared to standard care alone (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.93 to 1.08; 2 RCTs, 11,445 participants; moderate-certainty evidence). Worsening of clinical status: colchicine plus standard care probably results in little to no difference in worsening of clinical status assessed as new need for invasive mechanical ventilation or death compared to standard care alone (RR 1.02, 95% CI 0.96 to 1.09; 2 RCTs, 10,916 participants; moderate-certainty evidence). Improvement of clinical status: colchicine plus standard care probably results in little to no difference in improvement of clinical status, assessed as number of participants discharged alive up to day 28 without clinical deterioration or death compared to standard care alone (RR 0.99, 95% CI 0.96 to 1.01; 1 RCT, 11,340 participants; moderate-certainty evidence). Quality of life, including fatigue and neurological status: we identified no studies reporting this outcome. Adverse events: the evidence is very uncertain about the effect of colchicine on adverse events compared to placebo (RR 1.00, 95% CI 0.56 to 1.78; 1 RCT, 72 participants; very low-certainty evidence). Serious adverse events: the evidence is very uncertain about the effect of colchicine plus standard care on serious adverse events compared to standard care alone (0 events observed in 1 RCT of 105 participants; very low-certainty evidence). Treatment of non-hospitalised people with asymptomatic SARS-CoV-2 infection or mild COVID-19 All-cause mortality: the evidence is uncertain about the effect of colchicine on all-cause mortality at 28 days (Peto odds ratio (OR) 0.57, 95% CI 0.20 to 1.62; 1 RCT, 4488 participants; low-certainty evidence). Admission to hospital or death within 28 days: colchicine probably slightly reduces the need for hospitalisation or death within 28 days compared to placebo (RR 0.80, 95% CI 0.62 to 1.03; 1 RCT, 4488 participants; moderate-certainty evidence). Symptom resolution: we identified no studies reporting this outcome. Quality of life, including fatigue and neurological status: we identified no studies reporting this outcome. Adverse events: the evidence is uncertain about the effect of colchicine on adverse events compared to placebo . Results are from one RCT reporting treatment-related events only in 4412 participants (low-certainty evidence). Serious adverse events: colchicine probably slightly reduces serious adverse events (RR 0.78, 95% CI 0.61 to 1.00; 1 RCT, 4412 participants; moderate-certainty evidence). Colchicine versus another active treatment (e.g. corticosteroids, anti-viral drugs, monoclonal antibodies) No studies evaluated this comparison. Different formulations, doses, or schedules of colchicine No studies assessed this.
    AUTHORS' CONCLUSIONS: Based on the current evidence, in people hospitalised with moderate to severe COVID-19 the use of colchicine probably has little to no influence on mortality or clinical progression in comparison to placebo or standard care alone. We do not know whether colchicine increases the risk of (serious) adverse events. We are uncertain about the evidence of the effect of colchicine on all-cause mortality for people with asymptomatic infection or mild disease. However, colchicine probably results in a slight reduction of hospital admissions or deaths within 28 days, and the rate of serious adverse events compared with placebo. None of the studies reported data on quality of life or compared the benefits and harms of colchicine versus other drugs, or different dosages of colchicine. We identified 17 ongoing and 11 completed but not published RCTs, which we expect to incorporate in future versions of this review as their results become available. Editorial note: due to the living approach of this work, we monitor newly published results of RCTs on colchicine on a weekly basis and will update the review when the evidence or our certainty in the evidence changes.
    DOI:  https://doi.org/10.1002/14651858.CD015045
  22. J Clin Neurosci. 2021 Nov;pii: S0967-5868(21)00446-X. [Epub ahead of print]93 48-53
      Type-II odontoid fractures are common and highly morbid injuries, particularly among elderly patients. However, few risk stratification resources exist to predict outcomes and guide management decision making. Frailty indices have been increasingly utilized for these purposes in elective surgery, but have not been assessed for trauma. A single-center prospective trauma registry identified patients aged ≥ 80 years with type-II odontoid fractures. Frailty was the independent variable, using three independent indices: modified-5-item frailty (mFI-5), modified Charlson comorbidity (mCCI), and Davies. 97 patients had complete frailty data and sufficient follow up information, with median mIF-5 of 2 (range 0-4; 34 frail, mFI-5 > 2), median mCCI score of 6 (range 4-14), and median Davies score of 2 (range 0-7). For all indices, increasing score was associated with mortality, mIF-5 (HR = 1.76, 95%CI = 1.06-2.88), mCCI (HR = 1.10, 95%CI = 1.01-1.20), and Davies scores (HR = 1.21, 95%CI = 1.08-1.37). Median post-injury survival among patients with mIF-5 of ≤ 2 was 10-fold longer than patients with mIF-5 of > 2 (70 vs. 710 days, p = 0.0026). After adjusting for initial treatment strategy, frailty status remained an independent predictor of patient mortality; mIF-5 (HR = 1.72, 95%CI = 1.02-2.80), mCCI (HR = 1.10, 95%CI = 1.01-1.20), and Davies scores (HR = 1.21, 95%CI = 1.08-1.37). Among octogenarian patients with type-II odontoid fractures, frailty was associated with increased mortality, independent of treatment strategy.
    Keywords:  Davies; Elderly; Frailty; Spinal fracture; Type-II odontoid fracture; modified Charlson comorbidity (mCCI); modified-5-item frailty (mFI-5)
    DOI:  https://doi.org/10.1016/j.jocn.2021.08.027
  23. Am J Nurs. 2021 Nov 01. 121(11): 44-49
      This article is the first in a new series, Supporting Family Caregivers in the 4Ms of an Age-Friendly Health System, published in collaboration with the AARP Public Policy Institute as part of the ongoing Supporting Family Caregivers: No Longer Home Alone series. The 4Ms of an Age-Friendly Health System (What Matters, Medication, Mentation, and Mobility) is an evidence-based framework for assessing and acting on critical issues in the care of older adults across settings and transitions of care. Engaging the health care team, including older adults and their family caregivers, with the 4Ms framework can help to ensure that every older adult gets the best care possible, is not harmed by health care, and is satisfied with the care they receive. The articles in this new series present considerations for implementing the 4Ms framework in the inpatient hospital setting and incorporating family caregivers in doing so. Resources for both nurses and family caregivers, including a series of accompanying videos developed by AARP and the Rush Center for Excellence in Aging and funded by the John A. Hartford Foundation, are also provided. Nurses should read the articles first, so they understand how best to help family caregivers. Then they can refer caregivers to the informational tear sheet-Guide to the 4Ms of an Age-Friendly Health System for Family Caregivers-and instructional videos, encouraging them to ask questions. For additional information, see Resources for Nurses.
    DOI:  https://doi.org/10.1097/01.NAJ.0000799016.07144.0d
  24. Aging Cell. 2021 Oct 16. e13492
      Epigenetic alterations are a hallmark of aging and age-related diseases. Computational models using DNA methylation data can create "epigenetic clocks" which are proposed to reflect "biological" aging. Thus, it is important to understand the relationship between predictive clock sites and aging biology. To do this, we examined over 450,000 methylation sites from 9,699 samples. We found ~20% of the measured genomic cytosines can be used to make many different epigenetic clocks whose age prediction performance surpasses that of telomere length. Of these predictive sites, the average methylation change over a lifetime was small (~1.5%) and these sites were under-represented in canonical regions of epigenetic regulation. There was only a weak association between "accelerated" epigenetic aging and disease. We also compare tissue-specific and pan-tissue clock performance. This is critical to applying clocks both to new sample sets in basic research, as well as understanding if clinically available tissues will be feasible samples to evaluate "epigenetic aging" in unavailable tissues (e.g., brain). Despite the reproducible and accurate age predictions from DNA methylation data, these findings suggest they may have limited utility as currently designed in understanding the molecular biology of aging and may not be suitable as surrogate endpoints in studies of anti-aging interventions. Purpose-built clocks for specific tissues age ranges or phenotypes may perform better for their specific purpose. However, if purpose-built clocks are necessary for meaningful predictions, then the utility of clocks and their application in the field needs to be considered in that context.
    Keywords:  Aging; bioinformatics; epigenetic clocks; epigenetics
    DOI:  https://doi.org/10.1111/acel.13492
  25. Ageing Res Rev. 2021 Oct 15. pii: S1568-1637(21)00235-X. [Epub ahead of print] 101488
      Ageing is characterised by a physical decline in biological functioning which results in a progressive risk of mortality with time. As a biological phenomenon, it is underpinned by the dysregulation of a myriad of complex processes. Recently, however, ever-increasing evidence has associated epigenetic mechanisms, such as DNA methylation (DNAm) with age-onset pathologies, including cancer, cardiovascular disease, and Alzheimer's disease. These diseases compromise healthspan. Consequently, there is a medical imperative to understand the link between epigenetic ageing, and healthspan. Evolutionary theory provides a unique way to gain new insights into epigenetic ageing and health. This review will: (1) provide a brief overview of the main evolutionary theories of ageing; (2) discuss recent genetic evidence which has revealed alleles that have pleiotropic effects on fitness at different ages in humans; (3) consider the effects of DNAm on pleiotropic alleles, which are associated with age related disease; (4) discuss how age related DNAm changes resonate with the mutation accumulation, disposable soma and programmed theories of ageing; (5) discuss how DNAm changes associated with caloric restriction intersect with the evolution of ageing; and (6) conclude by discussing how evolutionary theory can be used to inform investigations which quantify age-related DNAm changes which are linked to age onset pathology.
    Keywords:  Ageing; DNA methylation; epigenetics; evolution
    DOI:  https://doi.org/10.1016/j.arr.2021.101488
  26. Age Ageing. 2021 Oct 18. pii: afab203. [Epub ahead of print]
      
    Keywords:  frail older people; hospitals; risk
    DOI:  https://doi.org/10.1093/ageing/afab203
  27. Nutrients. 2021 Oct 13. pii: 3579. [Epub ahead of print]13(10):
       BACKGROUND: Time restricted feeding (TRF) refers to dietary interventions in which food access is limited during a specific timeframe of the day. TRFs have proven useful in improving metabolic health in adult subjects with obesity. Their beneficial effects are mediated, in part, through modulating the circadian rhythm. Nevertheless, the translation of these dietary interventions onto obese/overweight children and adolescents remains uncharacterized. The objective of this study is to explore the feasibility of temporal dietary interventions for improving metabolic health in the context of childhood obesity.
    METHODS: We have previously developed a mouse model of early adiposity (i.e., childhood obesity) through litter size reduction. Mice raised in small litters (SL) became obese as early as by two weeks of age, and as adults, they developed several obesity-related co-morbidities, including insulin resistance, glucose intolerance and hepatic steatosis. Here, we explored whether two independent short-term chrono-nutritional interventions might improve metabolic health in 1-month-old pre-pubertal SL mice. Both TRFs comprised 8 h feeding/14 h fasting. In the first one (TRF1) Control and SL mice had access to the diet for 8 h during the dark phase. In the second intervention (TRF2) food was available during the light:dark transitions.
    RESULTS: TRF1 did not alter food intake nor ameliorate adiposity in SL-TRF1. In contrast, SL-TRF2 mice showed unintentional reduction of caloric intake, which was accompanied by reduced total body weight and adiposity. Strikingly, hepatic triglyceride content was completely normalized in SL-TRF1 and SL-TRF2 mice, when compared to the ad lib-fed SL mice. These effects were partially mediated by (i) clock-dependent signals, which might modulate the expression of Pparg or Cpt1a, and (ii) clock-independent signals, such as fasting itself, which could influence Fasn expression.
    CONCLUSIONS: Time-restricted feeding is an effective and feasible nutritional intervention to improve metabolic health, namely hepatic steatosis, in a model of childhood obesity. These data open new avenues for future safe and efficient chrono-nutritional interventions aimed to improve metabolic health in children with overweight/obesity.
    Keywords:  childhood obesity; circadian rhythm; non-alcoholic fatty liver disease; pubertal nutritional intervention; small litter; time-restricted feeding
    DOI:  https://doi.org/10.3390/nu13103579
  28. Cells. 2021 Sep 30. pii: 2603. [Epub ahead of print]10(10):
      Nucleotides are essential to cell growth and survival, providing cells with building blocks for DNA and RNA, energy carriers, and cofactors. Mitochondria have a critical role in the production of intracellular ATP and participate in the generation of intermediates necessary for biosynthesis of macromolecules such as purines and pyrimidines. In this review, we highlight the role of purine and mitochondrial metabolism in cancer and how their intersection influences cancer progression, especially in ovarian cancer. Additionally, we address the importance of metabolic rewiring in cancer and how the evolving landscape of purine synthesis and mitochondria inhibitors can be potentially exploited for cancer treatment.
    Keywords:  amino acids; cancers; metabolic reprogramming; mitochondrial metabolism; purines
    DOI:  https://doi.org/10.3390/cells10102603
  29. Environ Health Prev Med. 2021 Oct 20. 26(1): 105
       BACKGROUND: How community-based group resistance exercises affect the transition from robustness to frailty remains unclear. Thus, we conducted a retrospective cohort study to determine whether the trajectory from robustness to frailty over age differed depending on the duration of participation in group exercises.
    METHODS: We analyzed the Kihon Checklist (KCL) score of community-dwelling elderly residents of Sumoto city, Hyogo prefecture, who participated in community-based group resistance exercises between April 2010 and December 2019. Finally, 2567 older individuals were analyzed using multilevel modeling. The explanatory variables of interest were the frailty score measured using the KCL for each individual, where 0-3, 4-7, and ≥8 points denoted robustness, pre-frailty, and frailty, respectively. We considered age, sex, systolic blood pressure, pulse, duration of participation, and change in KCL score from baseline as possible confounders. Participants were classified as follows based on the duration of participation in the exercises: <3 times, short-term participation group; 4-6 times; mid-term participation group; and 7-13 times, long-term participation group. The mean duration from the baseline physical test for the total sample was 2.35 years (SD=2.51).
    RESULTS: The participants' mean total KCL score at baseline was 4.9±3.7. Multilevel modeling analysis revealed that the KCL scores changed by 0.82 points for each additional year of age (p<0.001) and changed by - 0.93 points for long-term participate group (p<0.001). The Estimated Marginal Means (EMM) of the KCL score was 3.98 (95%CI: 3.69, 4.28) points in the short-term participation group and was significantly worse than that of the long-term participation group at 70 years of age (p=0.001). The EMM was 4.49 (95%CI: 4.24, 4.74) at 75 years of age in the mid-term participation group and was significantly worse than that of the long-term participation group. The EMM was 3.87 (95%CI: 3.57, 4.16) in the long-term participation group and significantly better than that of the short-term (p<0.001) and mid-term (p=0.002) participation groups.
    CONCLUSION: Participation in community-based group resistance exercises prolongs the transition from robustness to frailty. The improved KCL scores at baseline in the long-term participation group remained in the robust range at 75 years of age, which suggests the importance of initiating participation before the onset of functional decline.
    Keywords:  Community-dwelling older adults; Frailty; Kihon Checklist; Lively 100-years-old physical exercise
    DOI:  https://doi.org/10.1186/s12199-021-01028-x
  30. Int Immunol. 2021 Oct 20. pii: dxab092. [Epub ahead of print]
      Most lineages of blood cells, including immune cells are generated from hematopoietic stem cells (HSCs) in bone marrow throughout adult life. Since HSCs cannot expand on their own, they require and contact the special microenvironments, termed niches for their maintenance. HSC niches comprise supportive cells that provide adjacent HSCs with critical signals, including cytokines. Although bone marrow microenvironments have been thought to be complex, recent studies have demonstrated that the bone marrow-specific population of fibroblastic reticular cells with long processes, termed CXC chemokine ligand 12 (CXCL12)-abundant reticular (CAR) cells, which overlap strongly with leptin receptor (LepR)-expressing (LepR +) cells, is the major cellular component of niches for HSCs and lymphoid progenitors. CAR cells have salient features, expressing much higher levels of critical HSC niche factors than any other cell populations and function as self-renewing mesenchymal stem cells. Human counterpart of CAR cells is present and affected in diseases, including leukemia. Foxl1 + telocytes recently identified as the niche for intestinal stem cells share some features with CAR cells, suggesting that CAR cells are prototypical fibroblastic reticular cells creating niche for long-lived cells, including tissue stem cells and memory lymphocytes. These findings provided the basis for future mechanistic studies on the crosstalk between hematopoietic cells and microenvironments in both health and disease.
    Keywords:  B cells; HSCs; lymphopoiesis; mesenchymal stem cells; microenvironments
    DOI:  https://doi.org/10.1093/intimm/dxab092
  31. Int J Environ Res Public Health. 2021 Oct 14. pii: 10776. [Epub ahead of print]18(20):
      Changing the food form for older adults requiring nursing care from a regular to dysphagia diet is thought to impact their nutritional status. We assessed the association between changes in food form and weight loss over 1 year in older adults. Older adults residing in long-term care facilities in Japan (n = 455) who participated in the baseline (2018) and follow-up (2019) surveys were divided into two groups (regular diet, n = 284; dysphagia diet, n = 171). The regular diet group was further divided into the weight loss (n = 80; weight loss ≥5% over 1 year) and weight maintenance (n = 204; weight loss <5%) groups. After 1 year, the Barthel Index significantly decreased, and the proportion of participants who switched from a regular diet to a dysphagia diet significantly increased in the weight loss group than in the weight maintenance group. Multivariate logistic regression analysis found that Barthel index variation (odds ratio (OR): 0.97, 95% confidence interval (CI): 0.94‒0.99), change from a regular diet to a dysphagia diet (OR: 4.41, 95% CI: 1.87‒10.41), and body weight at baseline (OR = 1.06, 95% CI: 1.01‒1.11) were significantly associated with weight loss. Our results suggest that maintaining the food form inhibits weight loss and improves health outcomes in older adults.
    Keywords:  food form; long-term care facility; nursing care; oral function; swallowing function; weight loss
    DOI:  https://doi.org/10.3390/ijerph182010776
  32. Cells. 2021 Oct 16. pii: 2776. [Epub ahead of print]10(10):
      Protein hydrolysate injection (PH) is a sterile solution of hydrolyzed protein and sorbitol that contains 17 amino acids and has a molecular mass of 185.0-622.0 g/mol. This study investigated the effect of PH on hematopoietic function in K562 cells and mice with cyclophosphamide (CTX)-induced hematopoietic dysfunction. In these myelosuppressed mice, PH increased the number of hematopoietic cells in the bone marrow (BM) and regulated the concentration of several factors related to hematopoietic function. PH restored peripheral blood cell concentrations and increased the numbers of hematopoietic stem cells and progenitor cells (HSPCs), B lymphocytes, macrophages, and granulocytes in the BM of CTX-treated mice. Moreover, PH regulated the concentrations of macrophage colony stimulating factor (M-CSF), interleukin (IL)-2, and other hematopoiesis-related cytokines in the serum, spleen, femoral condyle, and sternum. In K562 cells, the PH-induced upregulation of hematopoiesis-related proteins was inhibited by transfection with M-CSF siRNA. Therefore, PH might benefit the BM hematopoietic system via the regulation of M-CSF expression, suggesting a potential role for PH in the treatment of hematopoietic dysfunction caused by cancer therapy.
    Keywords:  M-CSF; hematopoietic function; protein hydrolysate injection
    DOI:  https://doi.org/10.3390/cells10102776
  33. Biomedicines. 2021 Oct 09. pii: 1429. [Epub ahead of print]9(10):
      Individuals with type 2 diabetes mellitus are at greater risk of developing cancer and of dying from it. Both diseases are age-related, contributing to the impact of population aging on the long-term sustainability of health care systems in European Union countries. The purpose of this narrative review was to describe, from epidemiological, pathophysiological and preventive perspectives, the links between type 2 diabetes mellitus and the most prevalent cancers in these patients. Multiple metabolic abnormalities that may occur in type 2 diabetes mellitus, particularly obesity, could explain the increased cancer risk. In addition, the effectiveness of drugs commonly used to treat type 2 diabetes mellitus (e.g., metformin and thiazolidinediones) has been broadly evaluated in cancer prevention. Thus, a better understanding of the links between type 2 diabetes mellitus and cancer will help to identify the contributing factors and the pathophysiological pathways and to design personalized preventive strategies. The final goal is to facilitate healthy aging and the prevention of cancer and other diseases related with type 2 diabetes mellitus, which are among the main sources of disability and death in the European Union and worldwide.
    Keywords:  disease prevention; epidemiology; metformin; neoplasms; obesity; thiazolidinediones; type 2 diabetes mellitus
    DOI:  https://doi.org/10.3390/biomedicines9101429