bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2025–08–17
eight papers selected by
Ayesh Seneviratne, McMaster University
  1. The immune system offers a window into aging.
  2. Ischemic Stroke and the Biological Hallmarks of Aging.
  3. Immune surveillance of senescent cells in aging and disease.
  4. Metabolic regulation of immunological aging.
  5. Aging reshapes the adaptive immune system from healer to saboteur.
  6. Aging and anti-aging strategies: A review of past and future therapeutics.
  7. Association of Pre-Diagnostic Clonal Hematopoiesis of Indeterminate Potential With Prognosis Among Patients With Cancer.
  8. Restoring resident tissue macrophages to combat aging and cancer.
  1. Nat Aging. 2025 Aug;5(8): 1377
    The immune system offers a window into aging.
      
    DOI:  https://doi.org/10.1038/s43587-025-00948-5
  2. Aging Dis. 2024 Sep 30. 16(5): 2908-2936
    Ischemic Stroke and the Biological Hallmarks of Aging.
    Fangyuan Cheng, Bo Yan, Pan Liao, Han Gao, Zhenyu Yin, Dai Li, Ping Lei.
      With the advent of an aging population, the study of aging and related research has been increasingly prominent, focusing on how to fully understand and delay aging-a key concern for contemporary medical professionals. Stroke is an acute focal neurological deficit. Globally, ischemic stroke accounts for only 60-70% of all strokes, meanwhile, it is the second leading cause of death. With the introduction of the concept of biomarkers of ageing, the research of ischemic stroke or acute brain injury in relation to these biomarkers has remained fragmented. In this review, we aim to consolidate the current evidence, highlighting the intricate relationship between ischemic stroke and aging-related hallmarks during its occurrence. By providing a comprehensive overview, we hope to offer researchers a broader perspective on how acute injury mechanisms intertwine with aging. We hope to present a new viewpoint and a more complete evaluation framework for future research and exploration in the field of aging.
    DOI:  https://doi.org/10.14336/AD.2024.1059
  3. Nat Aging. 2025 Aug;5(8): 1415-1424
    Immune surveillance of senescent cells in aging and disease.
    Julia Majewska, Valery Krizhanovsky.
      Senescent cells are intrinsically immunogenic and can be eliminated by the immune system to facilitate tissue repair and regeneration. However, immune-mediated elimination is compromised with age, causing senescent cell accumulation in tissues, thus limiting healthspan and lifespan and promoting age-related diseases such as cancer. Here, we review how different components of the innate and adaptive immune systems, including natural killer cells, macrophages, neutrophils, dendritic cells, T cells and B cells, target senescent cells and how the intrinsic properties of senescent cells can lead to their escape from surveillance. We also discuss the phenomenon of senescence in immune cells themselves and how this affects the surveillance of senescent and cancerous cells. Finally, we touch on emerging therapeutic strategies to enhance the immunosurveillance of senescent cells, as understanding the molecular basis of senescence immunosurveillance and why its potency fails during aging may offer opportunities to treat senescence-mediated age-associated diseases and tissue dysfunction.
    DOI:  https://doi.org/10.1038/s43587-025-00910-5
  4. Nat Aging. 2025 Aug;5(8): 1425-1440
    Metabolic regulation of immunological aging.
    Hee-Hoon Kim, Vishwa Deep Dixit.
      All biological activities require energy through the intake and generation of metabolites. After reproductive age, altered metabolism, together with cellular and molecular perturbations in the immune system, are linked to organismal functional decline. Unresolved chronic inflammation originating from innate immune cells and loss of naive T cells with restriction of T cell receptor repertoire diversity emanating from age-related thymic involution are some of the mechanisms that limit healthspan and even lifespan. Here, we provide an overview of the hallmarks of immunological aging and synthesize how the immune system, coupled to cellular and organismal metabolism, controls disease susceptibility. Furthermore, we highlight the potential unifying immunometabolic mechanisms of various genetic, pharmacological and dietary interventions that may underlie lifespan-healthspan extension. Given that immune and metabolic systems are modifiable and targetable, understanding the role of myriads of organ-resident immune cells and the underlying metabolic mechanisms that cause dysfunction can have transformational potential for the health of older adults.
    DOI:  https://doi.org/10.1038/s43587-025-00921-2
  5. Nat Aging. 2025 Aug;5(8): 1393-1403
    Aging reshapes the adaptive immune system from healer to saboteur.
    Sandra Delgado-Pulido, Matthew J Yousefzadeh, Maria Mittelbrunn.
      The classical role of adaptive immunity as a protector against external threats has expanded to include its functions in cancer surveillance, tissue repair and regeneration, and, more recently, it has emerged as a regulator of the aging process. In this Perspective, we discuss the mechanisms by which the deterioration of adaptive immunity contributes to inflammaging, cellular senescence and age-associated pathologies. We propose that age-related changes in lymphocytes contribute to aging through two distinct mechanisms. First, adaptive immune function worsens with age, impairing immunosurveillance of damaged or senescent cells and diminishing tissue regenerative potential, thereby indirectly disrupting tissue homeostasis. This disruption is particularly important in the gut, where maintaining tissue and microbiota homeostasis is crucial for overall health during aging. Second, adaptive immune cells often acquire pro-inflammatory and autoaggressive phenotypes with age, directly driving tissue damage, promoting senescence and exacerbating inflammaging. Finally, we explore the therapeutic potential of strategies aimed at enhancing the protective functions of lymphocytes or modulating their pathogenic phenotypes to promote healthy aging.
    DOI:  https://doi.org/10.1038/s43587-025-00906-1
  6. Bioorg Med Chem. 2025 Aug 05. pii: S0968-0896(25)00281-0. [Epub ahead of print]129 118340
    Aging and anti-aging strategies: A review of past and future therapeutics.
    Yuqing Wei, Baichen Xiong, Zuoaoyun Song, Sheng Zhong, Na Zheng, Ao Zhang, Yao Chen, Haopeng Sun.
      Aging is a progressive degenerative state characterized by a gradual loss of physiological fitness, resulting in deteriorated functions and susceptibility to age-related diseases. With the progress of research on aging and age-related mechanisms, identifying effective anti-aging drugs has become a key focus. In this review, we summarize aging and its related signaling pathways and targets, mainly including clearance of senescent cells, NAD+ augmentation, anti-inflammatory and anti-oxidant defense, dysfunction of proteostasis and activation of telomerase. Furthermore, we collect advanced research progress of anti-aging agents and other strategies to delay aging and age-related diseases, and ultimately ameliorate lifespan and healthspan. Finally, we review anti-aging research and discuss potential strategies for aging intervention.
    Keywords:  Activation of telomerase; Aging; Anti-aging strategies; Anti-oxidant defense; Cellular senescence; NAD(+) augmentation; Therapeutic agent
    DOI:  https://doi.org/10.1016/j.bmc.2025.118340
  7. Am J Hematol. 2025 Aug 11.
    Association of Pre-Diagnostic Clonal Hematopoiesis of Indeterminate Potential With Prognosis Among Patients With Cancer.
    Xinyuan Liu, Hans-Olov Adami, Tove Wästerlid, Huiwen Xue, Maria Feychting, Karin E Smedby, Fang Fang, Qianwei Liu.
      Clonal hematopoiesis of indeterminate potential (CHIP) might impair prognosis of several cancer types. Since previous studies predominantly focused on CHIP after cancer diagnosis, little is known about whether CHIP prior to cancer diagnosis predicts outcome. We performed a prospective cohort study, including 63 486 patients with cancer during 2006 to 2022 in the UK Biobank, to evaluate the association between pre-diagnostic CHIP and survival of cancer patients. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox regression models. We identified 2860 patients with cancer and pre-diagnostic CHIP, and 60 626 cancer patients without CHIP. During a median follow-up of 4.2 years, 1162 patients died in the CHIP group (921 cancer-specific deaths), and 17 825 in the reference group (14 785 cancer-specific deaths). Cancer patients with pre-diagnostic CHIP exhibited a higher rate of overall death (HR 1.18, 95% CI: 1.11-1.25) and cancer-specific death (HR 1.17, 95% CI: 1.09-1.25) compared with the reference group. A significant association of both overall death and cancer-specific death was observed for myeloproliferative neoplasms, multiple myeloma, breast cancer, non-Hodgkin lymphoma, and acute myeloid leukemia/myelodysplastic syndromes. The increased rate of both overall death and cancer-specific death was noted for CHIP with TET2, SRSF2, or JAK2 mutation. These findings suggested extended clinical awareness in cancer patients with pre-diagnostic CHIP.
    Keywords:  cancer; clonal hematopoiesis; cohort study; epidemiology; survival
    DOI:  https://doi.org/10.1002/ajh.70028
  8. Nat Aging. 2025 Aug;5(8): 1383-1392
    Restoring resident tissue macrophages to combat aging and cancer.
    Matthew D Park, Nader Yatim, Jing Zhang, Byuri Angela Cho, Seong-Keun Yoo, Maximilian M Schaefer, Diego Chowell, Daniel J Puleston, Miriam Merad.
      Perturbations to the immune system influence organismal aging, yet identifying effective therapeutic targets that mitigate aging-related tissue decline or the pathogenesis of aging-related diseases, such as cancer, remains challenging. In this Perspective, we focus on the dysfunction and loss of resident tissue macrophages (RTMs) with aging of certain tissues, which promote local inflammation, compromise tissue health and contribute to tumorigenesis. The abnormal genesis of RTMs from the bone marrow is a defining hallmark of both healthy and unhealthy aging. So, we propose that restoring RTMs-either by reshaping their niche and rescuing local self-renewal or by rejuvenating aging-associated myelopoiesis in the bone marrow-should be a major objective of interventions to promote healthy aging. We summarize the body of work supporting this conceptual framework and outline key future directions for the development of versatile myeloid-targeting therapies.
    DOI:  https://doi.org/10.1038/s43587-025-00898-y
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