bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2025–02–23
seven papers selected by
Ayesh Seneviratne, McMaster University



  1. Cardiol Rev. 2025 Feb 19.
      Aging is a multifaceted biological process characterized by progressive physiological decline and increased susceptibility to diseases. Central to this process are molecular and cellular changes that contribute to hallmark features of aging, including mitochondrial dysfunction, genomic instability, telomere attrition, and cellular senescence. Emerging research highlights the role of nutrient deficiencies in accelerating aging, bringing dietary supplements such as taurine and berberine into focus. Taurine, a sulfur-containing amino acid, plays a critical role in cellular protection, osmoregulation, and antioxidant defense, with evidence linking its deficiency to cellular senescence, mitochondrial dysfunction, and stem cell exhaustion. Berberine, an isoquinoline alkaloid, exerts antiaging effects by modulating key signaling pathways, including adenosine monophosphate-activated protein kinase/mechanistic target of rapamycin and sirtuin 1, and promoting mitohormesis. This review explores the mechanisms by which taurine and berberine mitigate aging processes, highlighting their effects on cellular metabolism, stress response, and longevity. Animal studies demonstrate their potential to enhance health span and lifespan although human clinical trials remain limited. Future research should focus on elucidating their molecular pathways, evaluating their combined effects with other interventions such as caloric restriction, and optimizing dosage for clinical applications. Taurine and berberine represent promising therapeutic candidates for addressing fundamental aspects of aging and advancing strategies for healthy aging and lifespan extension.
    DOI:  https://doi.org/10.1097/CRD.0000000000000885
  2. Nat Rev Cardiol. 2025 Feb 19.
      Ageing of the cardiovascular system is associated with frailty and various life-threatening diseases. As global populations grow older, age-related conditions increasingly determine healthspan and lifespan. The circulatory system not only supplies nutrients and oxygen to all tissues of the human body and removes by-products but also builds the largest interorgan communication network, thereby serving as a gatekeeper for healthy ageing. Therefore, elucidating organ-specific and cell-specific ageing mechanisms that compromise circulatory system functions could have the potential to prevent or ameliorate age-related cardiovascular diseases. In support of this concept, emerging evidence suggests that targeting the circulatory system might restore organ function. In this Roadmap, we delve into the organ-specific and cell-specific mechanisms that underlie ageing-related changes in the cardiovascular system. We raise unanswered questions regarding the optimal design of clinical trials, in which markers of biological ageing in humans could be assessed. We provide guidance for the development of gerotherapeutics, which will rely on the technological progress of the diagnostic toolbox to measure residual risk in elderly individuals. A major challenge in the quest to discover interventions that delay age-related conditions in humans is to identify molecular switches that can delay the onset of ageing changes. To overcome this roadblock, future clinical trials need to provide evidence that gerotherapeutics directly affect one or several hallmarks of ageing in such a manner as to delay, prevent, alleviate or treat age-associated dysfunction and diseases.
    DOI:  https://doi.org/10.1038/s41569-025-01130-5
  3. J Parkinsons Dis. 2025 Feb 02. 1877718X251316552
      Parkinson's disease (PD) is the most common neurodegenerative movement disorder, affecting 1-2% of people over age 65. The risk of developing PD dramatically increases with advanced age, indicating that aging is likely a driving factor in PD neuropathogenesis. Several age-associated biological changes are also hallmarks of PD neuropathology, including mitochondrial dysfunction, oxidative stress, and neuroinflammation. Accumulation of senescent cells is an important feature of aging that contributes to age-related diseases. How age-related cellular senescence affects brain health and whether this phenomenon contributes to neuropathogenesis in PD is not yet fully understood. In this review, we highlight hallmarks of aging, including mitochondrial dysfunction, loss of proteostasis, genomic instability and telomere attrition in relation to well established PD neuropathological pathways. We then discuss the hallmarks of cellular senescence in the context of neuroscience and review studies that directly examine cellular senescence in PD. Studying senescence in PD presents challenges and holds promise for advancing our understanding of disease mechanisms, which could contribute to the development of effective disease-modifying therapeutics. Targeting senescent cells or modulating the senescence-associated secretory phenotype (SASP) in PD requires a comprehensive understanding of the complex relationship between PD pathogenesis and cellular senescence.
    Keywords:  Parkinson's disease; aging; cellular senescence; neurodegeneration; senolytic
    DOI:  https://doi.org/10.1177/1877718X251316552