bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2021–03–28
33 papers selected by
Ayesh Seneviratne, University of Toronto



  1. Blood. 2021 Mar 22. pii: blood.2020007876. [Epub ahead of print]
      Hematopoietic stem cells (HSCs) and distinct multipotent progenitor populations (MPP1-4) contained within the Lin- Sca-1+ c-Kit+ (LSK) compartment have previously been identified using diverse surface marker panels. Here, we phenotypically define and functionally characterize MPP5 (LSK CD34+ CD135- CD48- CD150-). Upon transplantation, MPP5 support initial emergency myelopoiesis followed by stable contribution to the lymphoid lineage. Since MPP5 are capable of generating MPP1-4, but not HSCs, they represent a dynamic and versatile component of the MPP network. To characterize all hematopoietic stem and progenitor cells (HSPCs), we performed RNA-seq analysis to identify specific transcriptomic landscapes of HSCs and MPP1-5. This was complemented by single-cell (sc) RNA-seq analysis of LSK cells to establish the differentiation trajectories from HSCs to MPP1-5. In agreement with the functional reconstitution activity, MPP5 are located immediately downstream of HSCs but upstream of the more committed MPP2-4. This study provides a comprehensive analysis of the LSK compartment, focusing on the functional and molecular characteristics of the newly defined MPP5 subset.
    DOI:  https://doi.org/10.1182/blood.2020007876
  2. Gut Microbes. 2021 Jan-Dec;13(1):13(1): 1-24
      The gut microbiota plays an important role in cardio-metabolic diseases with diet being among the strongest modulators of gut microbiota composition and function. Resistant dietary carbohydrates are fermented to short-chain fatty acids (SCFAs) by the gut bacteria. Fiber and omega-3 rich diets increase SCFAs production and abundance of SCFA-producing bacteria. Likewise, SCFAs can improve gut barrier integrity, glucose, and lipid metabolism, regulate the immune system, the inflammatory response, and blood pressure. Therefore, targeting the gut microbiota with dietary strategies leading to increased SCFA production may benefit cardio-metabolic health. In this review, we provide an overview of the association between diet, SCFAs produced by the gut microbiota and cardio-metabolic diseases. We first discuss the association between the human gut microbiota and cardio-metabolic diseases, then investigate the role of SCFAs and finally explore the beneficial effects of specific dietary interventions that can improve cardio-metabolic outcomes through boosting the SCFA production.
    Keywords:  Short-chain fatty acids; cardio-metabolic health; diet; fiber; gut microbiota; omega-3
    DOI:  https://doi.org/10.1080/19490976.2021.1897212
  3. Cell Stem Cell. 2021 Mar 16. pii: S1934-5909(21)00108-9. [Epub ahead of print]
      Age-related clonal hematopoiesis (CH) is a risk factor for malignancy, cardiovascular disease, and all-cause mortality. Somatic mutations in DNMT3A are drivers of CH, but decades may elapse between the acquisition of a mutation and CH, suggesting that environmental factors contribute to clonal expansion. We tested whether infection provides selective pressure favoring the expansion of Dnmt3a mutant hematopoietic stem cells (HSCs) in mouse chimeras. We created Dnmt3a-mosaic mice by transplanting Dnmt3a-/- and WT HSCs into WT mice and observed the substantial expansion of Dnmt3a-/- HSCs during chronic mycobacterial infection. Injection of recombinant IFNγ alone was sufficient to phenocopy CH by Dnmt3a-/- HSCs upon infection. Transcriptional and epigenetic profiling and functional studies indicate reduced differentiation associated with widespread methylation alterations, and reduced secondary stress-induced apoptosis accounts for Dnmt3a-/- clonal expansion during infection. DNMT3A mutant human HSCs similarly exhibit defective IFNγ-induced differentiation. We thus demonstrate that IFNγ signaling induced during chronic infection can drive DNMT3A-loss-of-function CH.
    Keywords:  CH; DNMT3A; bone marrow; clonal competition; clonal hematopoiesis; epigenetic regulation; hematopoietic stem cell; infection; interferon gamma; mycobacterial infection
    DOI:  https://doi.org/10.1016/j.stem.2021.03.002
  4. Nat Commun. 2021 03 23. 12(1): 1826
      Somatic mutations of ASXL1 are frequently detected in age-related clonal hematopoiesis (CH). However, how ASXL1 mutations drive CH remains elusive. Using knockin (KI) mice expressing a C-terminally truncated form of ASXL1-mutant (ASXL1-MT), we examined the influence of ASXL1-MT on physiological aging in hematopoietic stem cells (HSCs). HSCs expressing ASXL1-MT display competitive disadvantage after transplantation. Nevertheless, in genetic mosaic mouse model, they acquire clonal advantage during aging, recapitulating CH in humans. Mechanistically, ASXL1-MT cooperates with BAP1 to deubiquitinate and activate AKT. Overactive Akt/mTOR signaling induced by ASXL1-MT results in aberrant proliferation and dysfunction of HSCs associated with age-related accumulation of DNA damage. Treatment with an mTOR inhibitor rapamycin ameliorates aberrant expansion of the HSC compartment as well as dysregulated hematopoiesis in aged ASXL1-MT KI mice. Our findings suggest that ASXL1-MT provokes dysfunction of HSCs, whereas it confers clonal advantage on HSCs over time, leading to the development of CH.
    DOI:  https://doi.org/10.1038/s41467-021-22053-y
  5. Cell Rep. 2021 Mar 23. pii: S2211-1247(21)00208-4. [Epub ahead of print]34(12): 108894
      The process of hematopoiesis is subject to substantial ontogenic remodeling that is accompanied by alterations in cellular fate during both development and disease. We combine state-of-the-art mass spectrometry with extensive functional assays to gain insight into ontogeny-specific proteomic mechanisms regulating hematopoiesis. Through deep coverage of the cellular proteome of fetal and adult lympho-myeloid multipotent progenitors (LMPPs), common lymphoid progenitors (CLPs), and granulocyte-monocyte progenitors (GMPs), we establish that features traditionally attributed to adult hematopoiesis are conserved across lymphoid and myeloid lineages, whereas generic fetal features are suppressed in GMPs. We reveal molecular and functional evidence for a diminished granulocyte differentiation capacity in fetal LMPPs and GMPs relative to their adult counterparts. Our data indicate an ontogeny-specific requirement of myosin activity for myelopoiesis in LMPPs. Finally, we uncover an ontogenic shift in the monocytic differentiation capacity of GMPs, partially driven by a differential expression of Irf8 during fetal and adult life.
    Keywords:  Irf8; adult hematopoiesis; developmental hematopoiesis; fetal hematopoiesis; hematopoietic progenitor cells; lymphopoiesis; myelopoiesis; proteomics
    DOI:  https://doi.org/10.1016/j.celrep.2021.108894
  6. Curr Opin Nephrol Hypertens. 2021 May 01. 30(3): 361-368
       PURPOSE OF REVIEW: The benefits of sodium/glucose cotransporter 2 (SGLT2) inhibitors seem to extend beyond glycemic control. We review recent randomized trial evidence evaluating SGLT2 inhibition in nondiabetic settings, including in patients with chronic kidney disease (CKD) and heart failure (HF).
    RECENT FINDINGS: DAPA-CKD, DAPA-HF and EMPEROR-Reduced compared SGLT2 inhibitors to placebo, enrolling 5868 patients without diabetes. In DAPA-CKD, patients with an estimated glomerular filtration rate (eGFR) of 25-75 ml/min/1.73 m2 and macroalbuminuria irrespective of kidney disease aetiology had improved cardiovascular and kidney outcomes if randomized to receive SGLT2 inhibitors (primary composite endpoint: hazard ratio [HR] 0.61, 95% CI 0.51-0.72; absolute risk reduction [ARR] 5.3%). In DAPA-HF and EMPEROR-Reduced, participants with reduced ejection fraction (HFrEF) had improved cardiovascular outcomes when an SGLT2 inhibitor was added to guideline-directed medical therapy, mainly through a reduction in HF hospitalizations (HR 0.70, 95% CI 0.59-0.83; ARR 3.7% and HR 0.69, 95% CI 0.59-0.81; ARR 5.1% with dapagliflozin and empagliflozin, respectively). In all 3 trials, the benefits were not modified by diabetes, baseline eGFR or proteinuria.
    SUMMARY: SGLT2 inhibitors improve kidney and HF outcomes in patients with high-risk CKD and HFrEF, irrespective of diabetes. Clinicians should become more comfortable prescribing these medications as we await studies that may further broaden their indications.
    DOI:  https://doi.org/10.1097/MNH.0000000000000703
  7. J Invest Dermatol. 2021 Apr;pii: S0022-202X(20)32368-X. [Epub ahead of print]141(4S): 949-950
      
    DOI:  https://doi.org/10.1016/j.jid.2020.12.002
  8. Aging (Albany NY). 2021 Mar 19. 13
      We analyzed the effects of ginsenoside Rb1 on hyperlipidemic in model mice. Using stool, plasma and hepatic tissue samples, we observed that the genera Blautia and Allobaculum were increased and Turicibacter was decrease in Rb1-treated mice as compared to untreated model mice. Ether lipid metabolism, glycerolipid metabolism, and glyoxylate and dicarboxylate metabolism were differentially enriched between the Rb1 and model groups. Lipidomics revealed 169 metabolites differentially expressed between the model and Rb1 groups in a positive ion model and 58 in a negative ion model. These metabolites mainly participate in glycerophospholipid, linoleic acid, and alpha-linolenic acid metabolism. The main metabolites enriched in these three pathways were phosphatidylcholine, diacylglycerol and ceramide, respectively. In a transcriptome analysis, 766 transcripts were differentially expressed between the Rb1 and model groups. KEGG analysis revealed lysine degradation, inositol phosphate metabolism, and glycerophospholipid metabolism to be the main enriched pathways. Multiomics analysis revealed glycerophospholipid metabolism to be a common pathway and phosphatidylcholine the main metabolite differentially enriched between the Rb1 and model groups. Results from fecal transplanted germ-free mice suggest that to suppress hyperlipidemia, Rb1 regulates gut microbiota by regulating the synthesis and decomposition of phosphatidylcholine in glycerophospholipid metabolism, which in turn decreases serum total cholesterol.
    Keywords:  ginsenoside Rb1; hyperlipidemia; lipidomics; microbiome; transcriptome
    DOI:  https://doi.org/10.18632/aging.202728
  9. Best Pract Res Clin Haematol. 2021 Mar;pii: S1521-6926(21)00016-5. [Epub ahead of print]34(1): 101251
      Resistance to therapy continues to pose hurdles in the therapeutic management of acute myeloid leukemia (AML). Although the approval and development of therapies such as venetoclax, was expected to overcome this issue, resistance remains a common occurrence in AML treatment. This review has summarized evidence that will provide insights into acquired mutations that influence response to venetoclax therapy and the utility of novel combination approaches in improving outcomes.
    Keywords:  AML; Acute myeloid leukemia; Complete response (CR); Venetoclax
    DOI:  https://doi.org/10.1016/j.beha.2021.101251
  10. Cancer Lett. 2021 Mar 17. pii: S0304-3835(21)00111-7. [Epub ahead of print]507 80-88
      Vascular endothelial growth factor receptor 2 (VEGFR2) activating mutations are emerging as important oncogenic driver events. Understanding the biological implications of such mutations may help to pinpoint novel therapeutic targets. Here we show that activated VEGFR2 via the pro-oncogenic R1051Q mutation induces relevant metabolic changes in melanoma cells. The expression of VEGFR2R1051Q leads to higher energy metabolism and ATP production compared to control cells expressing VEGFR2WT. Furthermore, activated VEGFR2R1051Q augments the dependence on glutamine (Gln) of melanoma cells, thus increasing Gln uptake and their sensitivity to Gln deprivation and to inhibitors of glutaminase, the enzyme initiating Gln metabolism by cells. Overall, these results highlight Gln addiction as a metabolic vulnerability of tumors harboring the activating VEGFR2R1051Q mutation and suggest novel therapeutic approaches for those patients harboring activating mutations of VEGFR2.
    Keywords:  Energy metabolism; Glutamine; Mutation; VEGFR2
    DOI:  https://doi.org/10.1016/j.canlet.2021.03.007
  11. Sci Rep. 2021 Mar 26. 11(1): 7008
      Dietary fiber functions as a prebiotic to determine the gut microbe composition. The gut microbiota influences the metabolic functions and immune responses in human health. The gut microbiota and metabolites produced by various dietary components not only modulate immunity but also impact various organs. Although recent findings have suggested that microbial dysbiosis is associated with several respiratory diseases, including asthma, cystic fibrosis, and allergy, the role of microbiota and metabolites produced by dietary nutrients with respect to pulmonary disease remains unclear. Therefore, we explored whether the gut microbiota and metabolites produced by dietary fiber components could influence a cigarette smoking (CS)-exposed emphysema model. In this study, it was demonstrated that a high-fiber diet including non-fermentable cellulose and fermentable pectin attenuated the pathological changes associated with emphysema progression and the inflammatory response in CS-exposed emphysema mice. Moreover, we observed that different types of dietary fiber could modulate the diversity of gut microbiota and differentially impacted anabolism including the generation of short-chain fatty acids, bile acids, and sphingolipids. Overall, the results of this study indicate that high-fiber diets play a beneficial role in the gut microbiota-metabolite modulation and substantially affect CS-exposed emphysema mice. Furthermore, this study suggests the therapeutic potential of gut microbiota and metabolites from a high-fiber diet in emphysema via local and systemic inflammation inhibition, which may be useful in the development of a new COPD treatment plan.
    DOI:  https://doi.org/10.1038/s41598-021-86404-x
  12. Hepatology. 2021 Mar 25.
       BACKGROUND & AIMS: The CD47-signal regulatory protein alpha (SIRPα) signaling pathway plays important roles in immune homeostasis and tissue inflammatory response. Activation of the Hedgehog/SMO/Gli1 pathway regulates cell growth, differentiation, and immune function. However, it remains unknown whether and how the CD47-SIRPα interaction may regulate Hedgehog/SMO/Gli1 signaling in mesenchymal stem cell (MSC)-mediated immune regulation during sterile inflammatory liver injury.
    APPROACH & RESULTS: In a mouse model of ischemia/reperfusion (IR)-induced sterile inflammatory liver injury, we found that adoptive transfer of MSCs increased CD47 expression and ameliorated liver IRI. However, deletion of CD47 in MSCs exacerbated IR-induced liver damage, with increased serum ALT levels, macrophage/neutrophil infiltration, and pro-inflammatory mediators. MSC treatment augmented SIRPα, Hedgehog/SMO/Gli1, and Notch1 intracellular domain (NICD), whereas CD47-deficient MSC treatment reduced these gene expressions in IR-stressed livers. Moreover, disruption of myeloid SMO or Notch1 increased IR-triggered liver inflammation with diminished Gli1 and NICD but enhanced NEK7 and NLRP3 activation in MSC-transferred mice. Using a MSC/macrophage co-culture system, we found that MSC CD47 and macrophage SIRPα expression were increased after LPS stimulation. The CD47-SIRPα interaction increased macrophage Gli1 and NICD nuclear translocation, whereby NICD interacted with Gli1 and regulated its target gene Dvl2, which in turn inhibited NEK7/NLRP3 activity.
    CONCLUSIONS: The CD47-SIRPα signaling activates the Hedgehog/SMO/Gli1 pathway, which controls NEK7/NLRP3 activity through a direct interaction between Gli1 and NICD. NICD is a novel coactivator of Gli1, and the target gene Dvl2 regulated by the NICD-Gli1 complex is crucial for the modulation of NLRP3-driven inflammatory response in MSC-mediated immune regulation. Our findings provide novel potential therapeutic targets in MSC-mediated immunotherapy of sterile inflammatory liver injury.
    Keywords:  Dvl2; NICD; NLRP3; Notch; SIRPα
    DOI:  https://doi.org/10.1002/hep.31831
  13. Aging (Albany NY). 2021 Mar 23.
      
    Keywords:  aggregates; cancer; lipid droplets; mitochondria; protein homeostasis
    DOI:  https://doi.org/10.18632/aging.202883
  14. J Natl Compr Canc Netw. 2021 Mar 26. pii: jnccn20285. [Epub ahead of print] 1-10
       BACKGROUND: Gauging fitness remains a challenge among older adults with hematologic malignancies, and interventions to restore function are lacking. We pilot a structured exercise intervention and novel biologic correlates of aging using epigenetic clocks and markers of immunosenescence to evaluate changes in function and clinical outcomes.
    METHODS: Older adults (n=30) with hematologic malignancy actively receiving treatment were screened and enrolled in a 6-month exercise intervention, the Otago Exercise Programme (OEP). The impact of the OEP on geriatric assessment metrics and health-related quality of life were captured. Clinical outcomes of overall survival and hospital utilization (inpatient length of stay and emergency department use) in relationship to geriatric deficits were analyzed.
    RESULTS: Older adults (median age, 75.5 years [range, 62-83 years]) actively receiving treatment were enrolled in the OEP. Instrumental activities of daily living and physical health scores (PHS) increased significantly with the OEP intervention (median PHS: visit 1, 55 [range, 0-100]; visit 2, 70 [range, 30-100]; P<.01). Patient-reported Karnofsky performance status increased significantly, and the improvement was sustained (median [range]: visit 1, 80 [40-100]; visit 3, 90 [50-100]; P=.05). Quality of life (Patient-Reported Outcome Measurement Information System [PROMIS]) improved significantly by the end of the 6-month period (median [range]: visit 1, 32.4 [19.9-47.7]; visit 3, 36.2 [19.9-47.7]; P=.01]. Enhanced measures of gait speed and balance, using the Short Physical Performance Battery scores, were associated with a 20% decrease in risk of death (hazard ratio, 0.80; 95% CI, 0.65-0.97; P=.03) and a shorter hospital length of stay (decrease of 1.29 days; 95% CI, -2.46 to -0.13; P=.03). Peripheral blood immunosenescent markers were analyzed in relationship to clinical frailty and reports of mPhenoAge epigenetic analysis are preliminarily reported. Chronologic age had no relationship to overall survival, length of stay, or emergency department utilization.
    CONCLUSIONS: The OEP was effective in improving quality of life, and geriatric tools predicted survival and hospital utilization among older adults with hematologic malignancies.
    DOI:  https://doi.org/10.6004/jnccn.2020.7686
  15. Aging (Albany NY). 2021 Mar 19. 13
      The present study assessed the body composition trajectory of rats (N = 96) placed into 5 groups according to lifespan, using dual-energy x-ray absorptiometry every 6 months until end-of-life. A striking linearity between lifespan and bone mass percentage (not absolute bone mass) was observed. Long-lived rats show a higher bone mass percentage with a delayed insulin rise to a similar peak level as short-lived counterparts, followed by insulin declines and bone mass loss. Decreasing insulin after streptozotocin (STZ) injection caused a rapid bone mass loss (-10.5%) with a decreased 5-day survival rate to 35% in old rats (20 months). Insulin replacement to STZ-injected rats completely blocked bone mass loss and increased the survival rate to 71%. Normal old rats (20 months) had faster lean mass loss despite greater myofiber regeneration (centronucleation) compared with the young rats (4 months). Increased CD68+ and CD163+ cell infiltration into insulin-depleted muscle suggests a bone marrow cell exhaustion by aging muscle. Bone produces stem cells and phagocytes to continuously rejuvenate peripheral tissues. Our data suggests that aging and unsustainable life is associated with development of disproportionality between bone and the growing body size, partly due to insulin reversal from hyperinsulinemia during late life.
    Keywords:  cachexia; frailty; longevity; osteopenia; sarcopenia
    DOI:  https://doi.org/10.18632/aging.202727
  16. Best Pract Res Clin Haematol. 2021 Mar;pii: S1521-6926(21)00004-9. [Epub ahead of print]34(1): 101243
      Allogeneic transplantation remains the most definitive curative option for patients with acute myeloid leukemia (AML). However, given the median age of diagnosis of AML in the late 60s, patients and clinicians have been reluctant to offer transplant to many in the older population. In this age group, AML presents with higher risk molecular and cytogenetic phenotype and patients' comorbidities, performance status, frailty and life views all impact the decision-making about whether to proceed with transplantation. Recent analyses suggest promising outcomes and thus acknowledgement of chronological age should be tempered with assessments of performance status, frailty, donor availability and careful balancing of a patient's wishes, life goals and understanding of the risks before restricting access of older patients to the curative potential of allotransplantation.
    Keywords:  Age; Allogeneic transplant; Frailty; Non-relapse mortality
    DOI:  https://doi.org/10.1016/j.beha.2021.101243
  17. Cell Mol Life Sci. 2021 Mar 23.
      Extracellular NAD represents a key signaling molecule in different physiological and pathological conditions. It exerts such function both directly, through the activation of specific purinergic receptors, or indirectly, serving as substrate of ectoenzymes, such as CD73, nucleotide pyrophosphatase/phosphodiesterase 1, CD38 and its paralog CD157, and ecto ADP ribosyltransferases. By hydrolyzing NAD, these enzymes dictate extracellular NAD availability, thus regulating its direct signaling role. In addition, they can generate from NAD smaller signaling molecules, like the immunomodulator adenosine, or they can use NAD to ADP-ribosylate various extracellular proteins and membrane receptors, with significant impact on the control of immunity, inflammatory response, tumorigenesis, and other diseases. Besides, they release from NAD several pyridine metabolites that can be taken up by the cell for the intracellular regeneration of NAD itself. The extracellular environment also hosts nicotinamide phosphoribosyltransferase and nicotinic acid phosphoribosyltransferase, which inside the cell catalyze key reactions in NAD salvaging pathways. The extracellular forms of these enzymes behave as cytokines, with pro-inflammatory functions. This review summarizes the current knowledge on the extracellular NAD metabolome and describes the major biochemical properties of the enzymes involved in extracellular NAD metabolism, focusing on the contribution of their catalytic activities to the biological function. By uncovering the controversies and gaps in their characterization, further research directions are suggested, also to better exploit the great potential of these enzymes as therapeutic targets in various human diseases.
    Keywords:  Ectoenzymes; NAMPT; NAPRT; NPP1; Pyridine metabolites; Signaling proteins
    DOI:  https://doi.org/10.1007/s00018-020-03742-1
  18. Ageing Res Rev. 2021 Mar 23. pii: S1568-1637(21)00070-2. [Epub ahead of print] 101323
      Advancing age is accompanied by changes in the gut microbiota characterised by a loss of beneficial commensal microbes that is driven by intrinsic and extrinsic factors such as diet, medications, sedentary behaviour and chronic health conditions. Concurrently, ageing is accompanied by an impaired ability to mount a robust immune response, termed immunesenescence, and age-associated inflammation, termed inflammaging. The microbiome has been proposed to impact the immune system and is a potential determinant of healthy aging. In this review we summarise the knowledge on the impact of ageing on microbial dysbiosis, intestinal permeability, inflammaging, and the immune system and investigate whether dysbiosis of the gut microbiota could be a potential mechanism underlying the decline in immune function, overall health and longevity with advancing age. Furthermore, we examine the potential of altering the gut microbiome composition as a novel intervention strategy to reverse the immune ageing clock and possibly support overall good health during old age.
    Keywords:  Immunesenescence; ageing; inflammaging; microbiome
    DOI:  https://doi.org/10.1016/j.arr.2021.101323
  19. Atherosclerosis. 2021 Feb 23. pii: S0021-9150(21)00087-3. [Epub ahead of print]
      
    Keywords:  Atherosclerosis; Carbohydrates; Lipids
    DOI:  https://doi.org/10.1016/j.atherosclerosis.2021.02.015
  20. Oncol Rev. 2021 Feb 26. 15(1): 514
      The main anti-diabetic effect of metformin mediated through stimulation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) is the inhibition of hepatic gluconeogenesis and triggering glucose uptake in skeletal muscles. Additionally, some new pathways, besides the AMPK activation, were discovered, that can explain wide-range properties of metformin. All these properties are now attracting the attention of researchers in the fields other than diabetes and the drug has been reported to have anti-cancer, immunoregulatory and anti-aging effects. Among others, the beneficial effects of metformin in hematological disorders like leukemias, lymphomas, and multiple myeloma were reported. Despite a great progress in therapy, these diseases are still incurable in most cases. Thus, there is an urgent need to discover novel, less toxic and more effective drugs especially for older or chemotherapy-resistant patients. In this review article, the current findings on the anti-cancer effect of metformin together with underlying possible mechanisms in blood cancers are discussed. However. to evaluate precisely these promising effects of metformin, more studies are required, because many of the published results are preclinical.
    Keywords:  AKT/mTOR signaling pathway; Metformin; leukemia; lymphoma; multiple myeloma
    DOI:  https://doi.org/10.4081/oncol.2021.514
  21. J Cereb Blood Flow Metab. 2021 Mar 24. 271678X211000894
      Ischemic strokes are highly prevalent in the elderly population and are a leading cause of mortality and morbidity worldwide. The risk of ischemic stroke increases in advanced age, corresponding with a noted decrease in circulating insulin growth factor-1 (IGF-1). IGF-1 is a known neuroprotectant involved in embryonic development, neurogenesis, neurotransmission, cognition, and lifespan. Clinically, several studies have shown that reduced levels of IGF-1 correlate with increased mortality rate, poorer functional outcomes, and increased morbidities following an ischemic stroke. In animal models of ischemia, administering exogenous IGF-1 using various routes of administration (intranasal, intravenous, subcutaneous, or topical) at various time points prior to and following insult attenuates neurological damage and accompanying behavioral changes caused by ischemia. However, there are some contrasting findings in select clinical and preclinical studies. This review discusses the role of IGF-1 as a determinant factor of ischemic stroke outcomes, both within the clinical settings and preclinical animal models. Furthermore, the review provides insight on the role of IGF-1 in mechanisms and cellular processes that contribute to stroke damage.
    Keywords:   Somatomedin C; glia; ischemia; neurodegeneration; stroke
    DOI:  https://doi.org/10.1177/0271678X211000894
  22. Hist Philos Life Sci. 2021 Mar 25. 43(2): 45
      While aging research and policy aim to promote 'health' at all ages, there remains no convincing explanation of what this 'health' is. In this paper, I investigate whether we can find, implicit within the sciences of aging, a way to know what health is and how to measure it, i.e. a theory of health. To answer this, I start from scientific descriptions of aging and its modulators and then try to develop some generalizations about 'health' implicit within this research. After discussing some of the core aspects of aging and the ways in which certain models describe spatial and temporal features specific to both aging and healthy phenotypes, I then extract, explicate, and evaluate one potential construct of health in these models. This suggests a theory of health based on the landscape of optimized phenotypic trajectories. I conclude by considering why it matters for more candidate theories to be proposed and evaluated by philosophers and scientists alike.
    Keywords:  Costs and trade-offs; Hormesis; Phenotypic trajectory; Referent analysis; Sciences of aging; Theory of health
    DOI:  https://doi.org/10.1007/s40656-021-00402-w
  23. Am J Nurs. 2021 Apr 01. 121(4): 25
      Editor's note: The mission of Cochrane Nursing is to provide an international evidence base for nurses involved in delivering, leading, or researching nursing care. Cochrane Corner provides summaries of recent systematic reviews from the Cochrane Library. For more information, see https://nursing.cochrane.org.
    DOI:  https://doi.org/10.1097/01.NAJ.0000742496.64945.3b
  24. Science. 2021 Mar 26. pii: eaba4177. [Epub ahead of print]371(6536):
      The pathways that lead to the development of tissue-resident lymphocytes, including liver type 1 innate lymphoid cells (ILC1s), remain unclear. We show here that the adult mouse liver contains Lin-Sca-1+Mac-1+ hematopoietic stem cells derived from the fetal liver. This population includes Lin-CD122+CD49a+ progenitors that can generate liver ILC1s but not conventional natural killer cells. Interferon-γ (IFN-γ) production by the liver ILC1s themselves promotes the development of these cells in situ, through effects on their IFN-γR+ liver progenitors. Thus, an IFN-γ-dependent loop drives liver ILC1 development in situ, highlighting the contribution of extramedullary hematopoiesis to regional immune composition within the liver.
    DOI:  https://doi.org/10.1126/science.aba4177
  25. Front Pharmacol. 2021 ;12 593116
      Though cancer therapeutics can successfully eradicate cancerous cells, the effectiveness of these medications is mostly restricted to several deleterious side effects. Therefore, to alleviate these side effects, antioxidant supplementation is often warranted, reducing reactive species levels and mitigating persistent oxidative damage. Thus, it can impede the growth of cancer cells while protecting the normal cells simultaneously. Moreover, antioxidant supplementation alone or in combination with chemotherapeutics hinders further tumor development, prevents chemoresistance by improving the response to chemotherapy drugs, and enhances cancer patients' quality of life by alleviating side effects. Preclinical and clinical studies have been revealed the efficacy of using phytochemical and dietary antioxidants from different sources in treating chemo and radiation therapy-induced toxicities and enhancing treatment effectiveness. In this context, algae, both micro and macro, can be considered as alternative natural sources of antioxidants. Algae possess antioxidants from diverse groups, which can be exploited in the pharmaceutical industry. Despite having nutritional benefits, investigation and utilization of algal antioxidants are still in their infancy. This review article summarizes the prospective anticancer effect of twenty-three antioxidants from microalgae and their potential mechanism of action in cancer cells, as well as usage in cancer therapy. In addition, antioxidants from seaweeds, especially from edible species, are outlined, as well.
    Keywords:  algae; antioxidant; cancer; cancer therapy; dietary supplements; reactive species
    DOI:  https://doi.org/10.3389/fphar.2021.593116
  26. Nat Commun. 2021 Mar 26. 12(1): 1927
      Accumulating evidence suggests that chronic inflammation of metabolic tissues plays a causal role in obesity-induced insulin resistance. Yet, how specific endothelial factors impact metabolic tissues remains undefined. Bone morphogenetic protein (BMP)-binding endothelial regulator (BMPER) adapts endothelial cells to inflammatory stress in diverse organ microenvironments. Here, we demonstrate that BMPER is a driver of insulin sensitivity. Both global and endothelial cell-specific inducible knockout of BMPER cause hyperinsulinemia, glucose intolerance and insulin resistance without increasing inflammation in metabolic tissues in mice. BMPER can directly activate insulin signaling, which requires its internalization and interaction with Niemann-Pick C1 (NPC1), an integral membrane protein that transports intracellular cholesterol. These results suggest that the endocrine function of the vascular endothelium maintains glucose homeostasis. Of potential translational significance, the delivery of BMPER recombinant protein or its overexpression alleviates insulin resistance and hyperglycemia in high-fat diet-fed mice and Leprdb/db (db/db) diabetic mice. We conclude that BMPER exhibits therapeutic potential for the treatment of diabetes.
    DOI:  https://doi.org/10.1038/s41467-021-22130-2
  27. Front Nutr. 2021 ;8 656290
      A good nutritional status is important for maintaining normal body function and preventing or mitigating the dysfunction induced by internal or external factors. Nutritional deficiencies often result in impaired function, and, conversely, intakes at recommended levels can resume or further enhance body functions. An increasing number of studies are revealing that diet and nutrition are critical not only for physiology and body composition, but also have significant effects on mood and mental well-being. In particular, Western dietary habits have been the object of several research studies focusing on the relationship between nutrition and mental health. This review aims to summarize the current knowledge about the relationship between the intake of specific micro- and macronutrients, including eicosapentaenoic acid, docosahexaenoic acid, alpha-tocopherol, magnesium and folic acid, and mental health, with particular reference to their beneficial effect on stress, sleep disorders, anxiety, mild cognitive impairment, as well as on neuropsychiatric disorders, all significantly affecting the quality of life of an increasing number of people. Overall data support a positive role for the nutrients mentioned above in the preservation of normal brain function and mental well-being, also through the control of neuroinflammation, and encourage their integration in a well-balanced and varied diet, accompanied by a healthy lifestyle. This strategy is of particular importance when considering the global human aging and that the brain suffers significantly from the life-long impact of stress factors.
    Keywords:  alpha-tocopherol; docosahexaenoic acid; eicosapentaenoic acid; folic acid; inflammation; magnesium; mental health; well-being
    DOI:  https://doi.org/10.3389/fnut.2021.656290
  28. Best Pract Res Clin Haematol. 2021 Mar;pii: S1521-6926(21)00022-0. [Epub ahead of print]34(1): 101257
      New drug approvals now afford AML physicians a wider choice of initial treatment options than ever before. Although chemotherapy for AML is by no means ready to be replaced entirely by novel agents, the role of traditional cytotoxics in AML therapy is rapidly changing. In particular, biologically targeted agents such as the BCL2 inhibitor venetoclax and inhibitors of FLT3 and IDH mutations stand out as drugs likely to take AML therapy in important new directions. Maximum response and survival benefits likely require combinations of novel agents and chemotherapy or multiple novel agents together. The recently-published phase 3 VIALE-A study demonstrates a very successful example of a new combination approach, which led to venetoclax plus azacitidine establishing itself as the new standard of care for patients unfit for intensive chemotherapy. One could reasonably expect other subsets of AML to benefit from this regimen or other applications of venetoclax combinations. Building on this experience, venetoclax-based regimens also have the potential to replace standard intensive cytarabine/anthracycline "7&3" induction approach for some if not many patients who are fit for induction. This review will describe novel agents with the greatest potential for impactful frontline applications that will change the AML treatment paradigm.
    Keywords:  Acute myeloid leukemia; BLC2 inhibition; FLT3 inhibition; IDH inhibition; Novel therapeutics
    DOI:  https://doi.org/10.1016/j.beha.2021.101257
  29. Front Cell Dev Biol. 2021 ;9 616520
      Organismic aging is known to be controlled by genetic and environmental traits. Pathways involved in the control of cellular metabolism play a crucial role. Previously, we identified a role of PaCLPP, a mitochondrial matrix protease, in the control of the mitochondrial energy metabolism, aging, and lifespan of the fungal aging model Podospora anserina. Most surprisingly, we made the counterintuitive observation that the ablation of this component of the mitochondrial quality control network leads to lifespan extension. In the current study, we investigated the role of energy metabolism of P. anserina. An age-dependent metabolome analysis of the wild type and a PaClpP deletion strain verified differences and changes of various metabolites in cultures of the PaClpP mutant and the wild type. Based on these data, we generated and analyzed a PaSnf1 deletion mutant and a ΔPaSnf1/ΔPaClpP double mutant. In both mutants PaSNF1, the catalytic α-subunit of AMP-activated protein kinase (AMPK) is ablated. PaSNF1 was found to be required for the development of fruiting bodies and ascospores and the progeny of sexual reproduction of this ascomycete and impact mitochondrial dynamics and autophagy. Most interestingly, while the single PaSnf1 deletion mutant is characterized by a slight lifespan increase, simultaneous deletion of PaSnf1 and PaClpP leads to a pronounced lifespan extension. This synergistic effect is strongly reinforced in the presence of the mating-type "minus"-linked allele of the rmp1 gene. Compared to the wild type, culture temperature of 35°C instead of the standard laboratory temperature of 27°C leads to a short-lived phenotype of the ΔPaSnf1/ΔPaClpP double mutant. Overall, our study provides novel evidence for complex interactions of different molecular pathways involved in mitochondrial quality control, gene expression, and energy metabolism in the control of organismic aging.
    Keywords:  AMPK; CLP protease; Podospora anserina; RMP1; SNF1; aging; development
    DOI:  https://doi.org/10.3389/fcell.2021.616520