bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2025–10–12
ten papers selected by
Ayesh Seneviratne, McMaster University



  1. Circulation. 2025 Oct 07. 152(14): 975-977
      
    Keywords:  atherosclerosis; cardiovascular diseases; clonal hematopoiesis; inflammation, risk stratification, precision medicine; risk factor
    DOI:  https://doi.org/10.1161/CIRCULATIONAHA.125.075769
  2. Blood. 2025 Oct 07. pii: blood.2024026505. [Epub ahead of print]
      Aged hematopoietic stem cells (HSCs) expand in clusters over time, while reducing their regenerative capacity and their ability to preserve the homeostasis of the hematopoietic system. The expression of Notch ligands in the bone marrow (BM) niche is essential for hematopoiesis. However, the impact of Notch signaling for adult HSC function and its involvement in HSC aging remains controversial. Here we show that Notch activation in young HSCs is not homogeneous, and it is triggered by sinusoidal expression of the Notch ligand Jagged2 (Jag2). Sinusoidal Jag2 deletion in young mice recapitulates the decrease in Notch activity observed in aged HSCs and alters HSC divisional symmetry and fate priming, promoting myeloid-biased HSCs (My-HSCs) expansion. Mechanistically, our data reveals that upon decreasing sinusoidal Jag2 expression, HSCs themselves upregulate Jag2, which cis-inhibits Notch signaling, resulting in the expansion of My-HSCs and in reduced hematopoietic regeneration. Collectively, these findings identify the crosstalk between BM niche-driven and HSC intrinsic features in regulating HSC fate priming and regenerative potential and reveal an extrinsic Notch trans-activation to intrinsic cis-inhibition switch underlying HSC aging.
    DOI:  https://doi.org/10.1182/blood.2024026505
  3. Nat Rev Endocrinol. 2025 Oct 06.
      Translational research on cellular senescence has led to numerous early-phase clinical trials targeting senescent cells to treat, prevent or alleviate multiple disorders and diseases, including metabolic diseases and their comorbidities. Cellular senescence is a cell fate that occurs in response to stressors, including metabolic disruptions, and is one of the hallmarks (or pillars) of ageing. In their senescent state, cells cease proliferation and can develop a senescence-associated secretory and metabolic phenotype that contributes to the pathogenesis of metabolic dysfunction associated with obesity and ageing. Metabolic stress, which is central to the development of metabolic diseases, can trigger cellular senescence, thereby enabling a vicious cycle that exacerbates metabolic dysfunction. Therapies targeting senescent cells (senotherapeutics), either alone or in combination with other gerotherapies or lifestyle interventions, hold great promise for addressing the ongoing obesity epidemic and the need for improved therapies to prevent and treat metabolic diseases and their complications and comorbidities. In this Review, we discuss novel senotherapeutics, including challenges related to the translation of these therapies and the need to establish gerodiagnostic biomarkers to track the elimination of senescent cells, define eligibility and measure efficacy, as well as considerations for clinical trial design and execution.
    DOI:  https://doi.org/10.1038/s41574-025-01187-9
  4. Nat Aging. 2025 Oct 08.
      Within each cell, metabolite-sensing factors respond to coordinate metabolic homeostasis. How metabolic homeostasis is regulated intercellularly and how this may become dysregulated with age, however, remains underexplored. Here we describe a system regulated by a metabolite sensor, CtBP2. CtBP2 is secreted via exosomes in response to reductive metabolism, which is suppressed by oxidative stress. Exosomal CtBP2 administration extends lifespan in aged mice and improves healthspan in particular by reducing frailty. Mechanistically, we identify activation of CYB5R3 and AMPK downstream of exosomal CtBP2. Consistently, serum CtBP2 levels decrease with age and are negatively associated with cardiovascular disease incidence in humans yet are elevated in individuals from families with a history of longevity. Together our findings define a CtBP2-mediated metabolic system with potential for future clinical applications.
    DOI:  https://doi.org/10.1038/s43587-025-00973-4
  5. Front Aging. 2025 ;6 1521401
      
    Keywords:  aging; anti-aging; longevity; marriage; single; singlehood; sleep
    DOI:  https://doi.org/10.3389/fragi.2025.1521401
  6. Nat Aging. 2025 Oct 07.
      Aging is characterized by the progressive deterioration of tissue structure and function, leading to increased vulnerability to diseases. Senescent cells (SCs) accumulate with age, but how the immune system regulates their burden is unclear. Here we show that CD4 T cells differentiate into Eomesodermin (Eomes)+CCL5+ T lymphocytes (CD4-Eomes) in a SC-rich environment and that a reduction in the SC load, achieved using senolytic drugs, was sufficient to halt this differentiation. We further demonstrate that eliminating CD4-Eomes cells at advanced age by selectively deleting the Eomes transcription factor in CD4 T cells results in increased accumulation of SCs, profound physical deterioration and a decreased lifespan. In liver cirrhosis, a model of localized chronic inflammation, CD4-Eomes cell elimination increased fibrosis, SC load and worsened the disease. Collectively, our findings demonstrate the fundamental role of CD4-Eomes cells in modulating tissue senescence, with implications for age-related diseases and longevity.
    DOI:  https://doi.org/10.1038/s43587-025-00953-8
  7. Curr Opin Cell Biol. 2025 Oct 07. pii: S0955-0674(25)00132-2. [Epub ahead of print]97 102594
      The skin is a dynamic, regenerative organ capable of withstanding diverse internal and external stresses, supported by tissue-resident stem cells. A complex signaling network regulates interactions between epidermal stem cells, dermal cells, immune cells, and the extracellular matrix to maintain tissue integrity. Disruptions in these signaling pathways can impair cellular communication, alter stem cell lineage commitment, and compromise epidermal stem cell identity, ultimately resulting in a loss of coordinated tissue function. In this review, we highlight recent insights into three key signaling factors-metabolic, mechanical, and inflammatory cues-that regulate epidermal stem cell behavior during homeostasis, regeneration, and aging. We further discuss how dysregulation of these pathways contributes to pathological skin remodeling and explore emerging intervention strategies targeting signaling molecules to restore epidermal stem cell function and skin health.
    DOI:  https://doi.org/10.1016/j.ceb.2025.102594