bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2023–07–30
twelve papers selected by
Ayesh Seneviratne, Western University



  1. bioRxiv. 2023 Jul 12. pii: 2023.07.12.548764. [Epub ahead of print]
      Age-associated clonal hematopoiesis (CH) occurs due to somatic mutations accrued in hematopoietic stem cells (HSCs) that confer a selective advantage in the context of aging. The mechanisms by which CH-mutant HSCs gain this advantage with aging are not comprehensively understood. Using unbiased transcriptomic approaches, we identify Oncostatin M (OSM) signaling as a candidate contributor to aging-driven Dnmt3a -mutant CH. We find that Dnmt3a -mutant HSCs from young mice do not functionally respond to acute OSM stimulation with respect to proliferation, apoptosis, hematopoietic engraftment, or myeloid differentiation. However, young Dnmt3a -mutant HSCs transcriptionally upregulate an inflammatory cytokine network in response to acute OSM stimulation including genes encoding IL-6, IL-1β and TNFα. In addition, OSM-stimulated Dnmt3a -mutant HSCs upregulate the anti-inflammatory genes Socs3, Atf3 and Nr4a1 , creating a negative feedback loop limiting sustained activation of the inflammatory network. In the context of an aged bone marrow (BM) microenvironment with chronically elevated levels of OSM, Dnmt3a -mutant HSCs upregulate pro-inflammatory genes but do not upregulate Socs3, Atf3 and Nr4a1 . Together, our work suggests that chronic inflammation with aging exhausts the regulatory mechanisms in young CH-mutant HSCs that resolve inflammatory states, and that OSM is a master regulator of an inflammatory network that contributes to age-associated CH.
    DOI:  https://doi.org/10.1101/2023.07.12.548764
  2. Aging Cell. 2023 Jul 27. e13942
      Current research on human aging has largely been guided by the milestone paper "hallmarks of aging," which were first proposed in the seminal 2013 paper by Lopez-Otin et al. Most studies have focused on one aging hallmark at a time, asking whether the underlying molecular perturbations are sufficient to drive the aging process and its associated phenotypes. More recently, researchers have begun to investigate whether aging phenotypes are driven by concurrent perturbations in molecular pathways linked to not one but to multiple hallmarks of aging and whether they present different patterns in organs and systems over time. Indeed, preliminary results suggest that more complex interactions between aging hallmarks must be considered and addressed, if we are to develop interventions that successfully promote healthy aging and/or delay aging-associated dysfunction and diseases. Here, we summarize some of the latest work and views on the interplay between hallmarks of aging, with a specific focus on mitochondrial dysfunction. Indeed, this represents a significant example of the complex crosstalk between hallmarks of aging and of the effects that an intervention targeted to a specific hallmark may have on the others. A better knowledge of these interconnections, of their cause-effect relationships, of their spatial and temporal sequence, will be very beneficial for the whole aging research field and for the identification of effective interventions in promoting healthy old age.
    Keywords:  ageing; aging; hallmarks of aging; mitochondria
    DOI:  https://doi.org/10.1111/acel.13942
  3. J Am Heart Assoc. 2023 Jul 25. e030603
      Clonal hematopoiesis of indeterminate potential (CHIP) is a common bone marrow abnormality induced by age-related DNA mutations, which give rise to proinflammatory immune cells. These immune cells exacerbate atherosclerotic cardiovascular disease and may induce or accelerate heart failure. The mechanisms involved are complex but point toward a central role for proinflammatory macrophages and an inflammasome-dependent immune response (IL-1 [interleukin-1] and IL-6 [interleukin-6]) in the atherosclerotic plaque or directly in the myocardium. Intracardiac inflammation may decrease cardiac function and induce cardiac fibrosis, even in the absence of atherosclerotic cardiovascular disease. The pathophysiology and consequences of CHIP may differ among implicated genes as well as subgroups of patients with heart failure, based on cause (ischemic versus nonischemic) and ejection fraction (reduced ejection fraction versus preserved ejection fraction). Evidence is accumulating that CHIP is associated with cardiovascular mortality in ischemic and nonischemic heart failure with reduced ejection fraction and involved in the development of heart failure with preserved ejection fraction. CHIP and corresponding inflammatory pathways provide a highly potent therapeutic target. Randomized controlled trials in patients with well-phenotyped heart failure, where readily available anti-inflammatory therapies are used to intervene with clonal hematopoiesis, may pave the way for a new area of heart failure treatment. The first clinical trials that target CHIP are already registered.
    Keywords:  atherosclerotic cardiovascular disease; clonal hematopoiesis; heart failure; inflammation
    DOI:  https://doi.org/10.1161/JAHA.123.030603
  4. BMB Rep. 2023 Jul 24. pii: 5964. [Epub ahead of print]
      The share of the population that is aging is growing rapidly. In an aging society, technologies and interventions that delay the aging process are of great interest. Dietary restriction (DR) is the most reproducible and effective nutritional intervention tested to date for delaying the aging process and prolonging the health span in animal models. Preventive effects of DR on age-related diseases have also been reported in human. In addition, highly conserved signaling pathways from small animal models to human mediate the effects of DR. Recent evidence has shown that the immune system is closely related to the effects of DR, and functions as a major mechanism of DR in healthy aging. This review discusses the effects of DR in delaying aging and preventing age-related diseases in animal, including human, and introduces the molecular mechanisms that mediate these effects. In addition, it reports scientific findings on the relationship between the immune system and DRinduced longevity. The review highlights the role of immunity as a potential mediator of the effects of DR on longevity, and provides insights into healthy aging in human.
  5. Stem Cells Dev. 2023 Jul 27.
      As the body ages, it experiences a gradual decline in the functioning of cells, tissues and systems, which eventually leads to dysfunction and increased susceptibility to disease. At the cellular level, a reduction in the activity or number of stem cells is an important feature of cell senescence, and such changes may also directly drive the aging of the organism. Thus, finding ways to prevent or even reverse stem cell senescence holds promise for the development of aging therapies in tissues and organisms. This review discusses the relationship between changes in stem cell senescence, tissues aging, and related diseases, focusing on four categories of tissue stem cells: hematopoietic stem cells (HSCs), mesenchymal stromal/stem cells (MSCs), intestinal stem cells (ISCs), and muscle stem cells (MuSCs).
    DOI:  https://doi.org/10.1089/scd.2023.0065
  6. NEJM Evid. 2023 May;2(5):
       Background: Clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS) are defined by somatic mutations in genes associated with myeloid neoplasms (MN) at a variant allele fraction (VAF) ≥ 0.02, in the absence and presence of cytopenia, respectively. CHIP/CCUS is highly prevalent in adults and defining predictors of MN risk would aid clinical management and research.
    Methods: We analyzed sequenced exomes of healthy UK Biobank (UKB) participants (n = 438,890) in separate derivation and validation cohorts. Genetic mutations, laboratory values, and MN outcomes were used in conditional probability-based recursive partitioning and Cox regression to determine predictors of incident MN. Combined statistical weights defined a clonal hematopoiesis risk score (CHRS). Independent CHIP/CCUS patient cohorts were used to test prognostic capability of the CHRS in the clinical setting.
    Results: Recursive partitioning distinguished CHIP/CCUS cases with 10-year probabilities of MN ranging from 0.0078 - 0.85. Multivariable analysis validated partitioning variables as predictors of MN. Key features, including single DNMT3A mutations, high risk mutations, ≥ 2 mutations, VAF ≥ 0.2, age ≥ 65 years, CCUS vs CHIP and red blood cell indices, influenced MN risk in variable direction. The CHRS defined low risk (n = 10018, 88.4%), intermediate risk (n = 1196, 10.5%), and high risk (n = 123, 1.1%) groups. In clinical cohorts, most MN events occurred in high risk CHIP/CCUS patients.
    Conclusions: The CHRS provides simple prognostic framework for CHIP/CCUS, distinguishing a high risk minority from the majority of CHIP/CCUS which has minimal risk for progression to MN.
    DOI:  https://doi.org/10.1056/evidoa2200310
  7. Biochim Biophys Acta Mol Basis Dis. 2023 Jul 25. pii: S0925-4439(23)00181-3. [Epub ahead of print] 166815
      Aging is characterized by progressive functional deterioration with increased risk of mortality. It is a complex biological process driven by a multitude of intertwined mechanisms such as increased DNA damage, chronic inflammation, and metabolic dysfunction. Sirtuins (SIRTs) are a family of NAD+-dependent enzymes that regulate fundamental biological functions from genomic stability and lifespan to energy metabolism and tumorigenesis. Of the seven mammalian SIRT isotypes (SIRT1-7), SIRT1 and SIRT6 are well-recognized for regulating signaling pathways related to aging. Herein, we review the protective role of SIRT1 and SIRT6 in aging-related diseases at molecular, cellular, tissue, and whole-organism levels. We also discuss the therapeutic potential of SIRT1 and SIRT6 modulators in the treatment of these diseases and challenges thereof.
    Keywords:  Aging; Aging-related diseases; SIRT1; SIRT6; Sirtuins
    DOI:  https://doi.org/10.1016/j.bbadis.2023.166815
  8. J Clin Invest. 2023 Jul 27. pii: e168597. [Epub ahead of print]
      Clonal hematopoiesis of indeterminate potential (CHIP) is associated with an increased risk of cardiovascular diseases (CVD), putatively via inflammasome activation. We pursued an inflammatory gene modifier scan for CHIP-associated CVD risk among 424,651 UK Biobank participants. CHIP was identified using whole exome sequencing data of blood DNA and modeled both as a composite and for common drivers (DNMT3A, TET2, ASXL1, and JAK2) separately. We developed predicted gene expression scores for 26 inflammasome-related genes and assessed how they modify CHIP-associated CVD risk. We identify IL1RAP as a potential key molecule for CHIP-associated CVD risk across genes and increased AIM2 gene expression leading to heightened JAK2- and ASXL1-associated CVD risks. We show that CRISPR-induced Asxl1 mutated murine macrophages have a particularly heightened inflammatory response to AIM2 agonism, associated with an increased DNA damage response, as well as increased IL-10 secretion, mirroring a CVD protective effect of IL10 expression in ASXL1 CHIP. Our study supports the role of inflammasomes in CHIP-associated CVD and provides new evidence to support gene-specific strategies to address CHIP-associated CVD risk.
    Keywords:  Cardiology; Cardiovascular disease; Genetics; Mouse models; Population genetics
    DOI:  https://doi.org/10.1172/JCI168597
  9. Eur J Haematol. 2023 Jul 25.
       BACKGROUND: The treatment of relapsed or refractory (R/R) acute myeloid leukaemia (AML) remains challenging and outcomes extremely poor. The introduction of venetoclax has transformed the treatment of AML and emerging data suggest that venetoclax-based therapy may enforce salvage treatment.
    MATERIALS AND METHODS: In this nationwide Danish retrospective study, we analysed treatment outcomes of venetoclax-based salvage treatment for R/R AML between 2019 and 2022. Only venetoclax-naive patients who had previously received treatment with intensive chemotherapy therapy were included.
    RESULTS: The cohort consisted of 43 R/R patients with a median age of 57 years. Nine (20.9%) were primary refractory and 34 (79.1%) patients had relapsed, including 21 after previous allogeneic stem cell transplantation. The overall response rate was 76.2% including 61.9% with composite complete remission (CRc: CR + CRi). Among CRc-responders with information on measurable residual disease (MRD), 8/13 (61.5%) obtained an MRD-negativity response. The overall survival was 9.3 months for all patients with an estimated 1-year overall survival of 34%. For CRc-responders the median overall survival was 13.3 months, and the median relapse-free survival was 12.8 months.
    CONCLUSION: Venetoclax-based salvage treatment for R/R AML produced high response rates; however, for most patients the response was of limited duration. This study is limited by an observational design and prone to selection bias.
    Keywords:  BCL-2; acute myeloid leukaemia; measurable residual disease; relapse/refractory; venetoclax
    DOI:  https://doi.org/10.1111/ejh.14046
  10. Front Cell Dev Biol. 2023 ;11 1204160
      Chronic inflammation is a common feature of aging and numerous diseases such as diabetes, obesity, and autoimmune syndromes and has been linked to the development of hematological malignancy. Blood-forming hematopoietic stem cells (HSC) can contribute to these diseases via the production of tissue-damaging myeloid cells and/or the acquisition of mutations in epigenetic and transcriptional regulators that initiate evolution toward leukemogenesis. We previously showed that the myeloid "master regulator" transcription factor PU.1 is robustly induced in HSC by pro-inflammatory cytokines such as interleukin (IL)-1β and limits their proliferative activity. Here, we used a PU.1-deficient mouse model to investigate the broader role of PU.1 in regulating hematopoietic activity in response to chronic inflammatory challenges. We found that PU.1 is critical in restraining inflammatory myelopoiesis via suppression of cell cycle and self-renewal gene programs in myeloid-biased multipotent progenitor (MPP) cells. Our data show that while PU.1 functions as a key driver of myeloid differentiation, it plays an equally critical role in tailoring hematopoietic responses to inflammatory stimuli while limiting expansion and self-renewal gene expression in MPPs. These data identify PU.1 as a key regulator of "emergency" myelopoiesis relevant to inflammatory disease and leukemogenesis.
    Keywords:  PU.1; hematopoiesis; hematopoietic progenitor cell; hematopoietic stem cell; inflammation; myelopoiesis
    DOI:  https://doi.org/10.3389/fcell.2023.1204160