bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2024‒02‒04
eleven papers selected by
Ayesh Seneviratne, Western University
  1. Clonal Hematopoiesis: Getting to the Heart of the Problem With Clone Size.
  2. SRCAP mutations drive clonal hematopoiesis through epigenetic and DNA repair dysregulation.
  3. The hallmarks of aging as a conceptual framework for health and longevity research.
  4. Epigenetic clock work ticks forward.
  5. Why human brain cells grow so slowly.
  6. Age-related motor deficits caused by clonal haematopoiesis-driven, monocyte-derived microglia.
  7. Metabolic regulation of the hallmarks of stem cell biology.
  8. Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation.
  9. Impact of frailty on outcomes of elderly patients undergoing percutaneous coronary intervention: A systematic review and meta-analysis.
  10. Elon Musk's Neuralink brain chip: what scientists think of first human trial.
  11. Mitophagy curtails cytosolic mtDNA-dependent activation of cGAS/STING inflammation during aging.
  1. JACC Heart Fail. 2024 Jan 21. pii: S2213-1779(24)00037-4. [Epub ahead of print]
    Clonal Hematopoiesis: Getting to the Heart of the Problem With Clone Size.
    Kenneth Walsh, Jesse D Cochran, Megan A Evans.
      
    Keywords:  biomarker; cardiovascular disease; clonal hematopoiesis; precision medicine; prognosis
    DOI:  https://doi.org/10.1016/j.jchf.2023.12.009
  2. Cell Stem Cell. 2024 Feb 01. pii: S1934-5909(24)00001-8. [Epub ahead of print]31(2): 275-277
    SRCAP mutations drive clonal hematopoiesis through epigenetic and DNA repair dysregulation.
    Chun-Wei Chen, Linda Zhang, Ravi Dutta, Abhishek Niroula, Peter G Miller, Christopher J Gibson, Alexander G Bick, Jaime M Reyes, Yi-Tang Lee, Ayala Tovy, Tianpeng Gu, Sarah Waldvogel, Yi-Hung Chen, Bryan J Venters, Pierre-Olivier Estève, Sriharsa Pradhan, Michael-Christopher Keogh, Pradeep Natarajan, Koichi Takahashi, Adam S Sperling, Margaret A Goodell.
      
    DOI:  https://doi.org/10.1016/j.stem.2024.01.001
  3. Front Aging. 2024 ;5 1334261
    The hallmarks of aging as a conceptual framework for health and longevity research.
    Antonio G Tartiere, José M P Freije, Carlos López-Otín.
      The inexorability of the aging process has sparked the curiosity of human beings since ancient times. However, despite this interest and the extraordinary scientific advances in the field, the complexity of the process has hampered its comprehension. In this context, The Hallmarks of Aging were defined in 2013 with the aim of establishing an organized, systematic and integrative view of this topic, which would serve as a conceptual framework for aging research. Ten years later and promoted by the progress in the area, an updated version included three new hallmarks while maintaining the original scope. The aim of this review is to determine to what extent The Hallmarks of Aging achieved the purpose that gave rise to them. For this aim, we have reviewed the literature citing any of the two versions of The Hallmarks of Aging and conclude that they have served as a conceptual framework not only for aging research but also for related areas of knowledge. Finally, this review discusses the new candidates to become part of the Hallmarks list, analyzing the evidence that supports whether they should or should not be incorporated.
    Keywords:  biomarkers; healthspan; lifespan; progeria; rejuvenation; senescence
    DOI:  https://doi.org/10.3389/fragi.2024.1334261
  4. Nat Aging. 2024 Jan 30.
    Epigenetic clock work ticks forward.
    C P Ryan, D W Belsky.
      
    DOI:  https://doi.org/10.1038/s43587-024-00570-x
  5. Nature. 2024 Jan 31.
    Why human brain cells grow so slowly.
    Shamini Bundell.
      
    Keywords:  Ageing; Cell biology; Epigenetics; Neuroscience
    DOI:  https://doi.org/10.1038/d41586-024-00280-9
  6. Nat Rev Immunol. 2024 Jan 30.
    Age-related motor deficits caused by clonal haematopoiesis-driven, monocyte-derived microglia.
    Austeja Baleviciute, Lily Keane.
      
    DOI:  https://doi.org/10.1038/s41577-024-00997-8
  7. Cell Stem Cell. 2024 Feb 01. pii: S1934-5909(24)00003-1. [Epub ahead of print]31(2): 161-180
    Metabolic regulation of the hallmarks of stem cell biology.
    Benjamin T Jackson, Lydia W S Finley.
      Stem cells perform many different functions, each of which requires specific metabolic adaptations. Over the past decades, studies of pluripotent and tissue stem cells have uncovered a range of metabolic preferences and strategies that correlate with or exert control over specific cell states. This review aims to describe the common themes that emerge from the study of stem cell metabolism: (1) metabolic pathways supporting stem cell proliferation, (2) metabolic pathways maintaining stem cell quiescence, (3) metabolic control of cellular stress responses and cell death, (4) metabolic regulation of stem cell identity, and (5) metabolic requirements of the stem cell niche.
    DOI:  https://doi.org/10.1016/j.stem.2024.01.003
  8. Cell Regen. 2024 Jan 31. 13(1): 2
    Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation.
    Xinhang Li, Yalin Zhu, Pilar Ruiz-Lozano, Ke Wei.
      The regenerative capacity of the adult mammalian heart remains a formidable challenge in biological research. Despite extensive investigations into the loss of regenerative potential during evolution and development, unlocking the mechanisms governing cardiomyocyte proliferation remains elusive. Two recent groundbreaking studies have provided fresh perspectives on mitochondrial-to-nuclear communication, shedding light on novel factors that regulate cardiomyocyte proliferation. The studies identified two mitochondrial processes, fatty acid oxidation and protein translation, as key players in restricting cardiomyocyte proliferation. Inhibition of these processes led to increased cell cycle activity in cardiomyocytes, mediated by reduction in H3k4me3 levels through accumulated α-ketoglutarate (αKG), and activation of the mitochondrial unfolded protein response (UPRmt), respectively. In this research highlight, we discuss the novel insights into mitochondrial-to-nuclear communication presented in these studies, the broad implications in cardiomyocyte biology and cardiovascular diseases, as well as the intriguing scientific questions inspired by the studies that may facilitate future investigations into the detailed molecular mechanisms of cardiomyocyte metabolism, proliferation, and mitochondrial-to-nuclear communications.
    Keywords:  ATF4; Cardiomyocyte; Cpt1b; FAO; H3k4me3; Mitochondria; Mrps5; Proliferation; UPRmt; αKG
    DOI:  https://doi.org/10.1186/s13619-024-00186-x
  9. World J Clin Cases. 2024 Jan 06. 12(1): 107-118
    Impact of frailty on outcomes of elderly patients undergoing percutaneous coronary intervention: A systematic review and meta-analysis.
    Shi-Shi Wang, Wang-Hao Liu.
      BACKGROUND: Frailty is a common condition in elderly patients who receive percutaneous coronary intervention (PCI). However, how frailty affects clinical outcomes in this group is unclear.AIM: To assess the link between frailty and the outcomes, such as in-hospital complications, post-procedural complications, and mortality, in elderly patients post-PCI.
    METHODS: The PubMed/MEDLINE, EMBASE, Cochrane Library, and Web of Science databases were screened for publications up to August 2023. The primary outcomes assessed were in-hospital and all-cause mortality, major adverse cardiovascular events (MACEs), and major bleeding. The Newcastle-Ottawa Scale was used for quality assessment.
    RESULTS: Twenty-one studies with 739693 elderly patients undergoing PCI were included. Frailty was consistently associated with adverse outcomes. Frail patients had significantly higher risks of in-hospital mortality [risk ratio: 3.45, 95% confidence interval (95%CI): 1.90-6.25], all-cause mortality [hazard ratio (HR): 2.08, 95%CI: 1.78-2.43], MACEs (HR: 2.92, 95%CI: 1.85-4.60), and major bleeding (HR: 4.60, 95%CI: 2.89-7.32) compared to non-frail patients.
    CONCLUSION: Frailty is a pivotal determinant in the prediction of risk of mortality, development of MACEs, and major bleeding in elderly individuals undergoing percutaneous coronary intervention.
    Keywords:  Elderly; Frailty; Meta-analysis; Percutaneous coronary intervention; Systematic review
    DOI:  https://doi.org/10.12998/wjcc.v12.i1.107
  10. Nature. 2024 Feb 02.
    Elon Musk's Neuralink brain chip: what scientists think of first human trial.
    Liam Drew.
      
    Keywords:  Brain; Neuroscience; Technology
    DOI:  https://doi.org/10.1038/d41586-024-00304-4
  11. Nat Commun. 2024 Jan 27. 15(1): 830
    Mitophagy curtails cytosolic mtDNA-dependent activation of cGAS/STING inflammation during aging.
    Juan Ignacio Jiménez-Loygorri, Beatriz Villarejo-Zori, Álvaro Viedma-Poyatos, Juan Zapata-Muñoz, Rocío Benítez-Fernández, María Dolores Frutos-Lisón, Francisco A Tomás-Barberán, Juan Carlos Espín, Estela Area-Gómez, Aurora Gomez-Duran, Patricia Boya.
      Macroautophagy decreases with age, and this change is considered a hallmark of the aging process. It remains unknown whether mitophagy, the essential selective autophagic degradation of mitochondria, also decreases with age. In our analysis of mitophagy in multiple organs in the mito-QC reporter mouse, mitophagy is either increased or unchanged in old versus young mice. Transcriptomic analysis shows marked upregulation of the type I interferon response in the retina of old mice, which correlates with increased levels of cytosolic mtDNA and activation of the cGAS/STING pathway. Crucially, these same alterations are replicated in primary human fibroblasts from elderly donors. In old mice, pharmacological induction of mitophagy with urolithin A attenuates cGAS/STING activation and ameliorates deterioration of neurological function. These findings point to mitophagy induction as a strategy to decrease age-associated inflammation and increase healthspan.
    DOI:  https://doi.org/10.1038/s41467-024-45044-1
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