bims-agimec Biomed News
on Aging mechanisms
Issue of 2024–08–11
seven papers selected by
Metin Sökmen, Ankara Üniversitesi
  1. Gut microbiota and healthy longevity.
  2. Targeting vascular senescence in cardiovascular disease with aging.
  3. Are immunosenescent T cells really senescent?
  4. Decoding molecular mechanisms: brain aging and Alzheimer's disease.
  5. Oxidative stress and aging: synergies for age related diseases.
  6. Ageing-related bone and immunity changes: insights into the complex interplay between the skeleton and the immune system.
  7. Implications of endoplasmic reticulum stress and autophagy in aging and cardiovascular diseases.
  1. Sci China Life Sci. 2024 Aug 02.
    Gut microbiota and healthy longevity.
    Jia Luo, Shan Liang, Feng Jin.
      Recent progress on the underlying biological mechanisms of healthy longevity has propelled the field from elucidating genetic modification of healthy longevity hallmarks to defining mechanisms of gut microbiota influencing it. Importantly, the role of gut microbiota in the healthy longevity of the host may provide unprecedented opportunities to decipher the plasticity of lifespan on a natural evolutionary scale and shed light on using microbiota-targeted strategies to promote healthy aging and combat age-related diseases. This review investigates how gut microbiota affects healthy longevity, focusing on the mechanisms through which gut microbiota modulates it. Specifically, we focused on the ability of gut microbiota to enhance the intestinal barrier integrity, provide protection from inflammaging, ameliorate nutrientsensing pathways, optimize mitochondrial function, and improve defense against age-related diseases, thus participating in enhancing longevity and healthspan.
    Keywords:  bile acids; gut microbiota; healthy aging; longevity; short-chain fatty acids; tryptophan metabolites
    DOI:  https://doi.org/10.1007/s11427-023-2595-5
  2. J Cardiovasc Aging. 2024 Apr;pii: 16. [Epub ahead of print]4(2):
    Targeting vascular senescence in cardiovascular disease with aging.
    Shelby A Hall, Lisa A Lesniewski.
      Aging is a major risk factor for atherosclerosis and cardiovascular disease (CVD). Two major age-associated arterial phenotypes, endothelial dysfunction and large elastic arterial stiffness, are autonomous predictors of future CVD diagnosis and contribute to the progression of CVD in older adults. Senescent cells lose the capacity to proliferate but remain metabolically active and secrete inflammatory factors termed senescence-associated secretory phenotype (SASP), leading to an increase in inflammation and oxidative stress. Accumulation of senescent cells is linked with the progression of age-related diseases and has been known to play a role in cardiovascular disease. In this brief review, we describe the characteristics and mechanisms of senescent cell accumulation and how senescent cells promote endothelial dysfunction and arterial stiffness. We focus on a range of novel therapeutic strategies aimed at reducing the burden of endothelial dysfunction leading to atherosclerosis through targeting senescent cells. Studies have begun to investigate a specific class of drugs that are able to selectively eliminate senescent cells, termed senolytics, which have shown great promise in reversing the aging phenotype and ameliorating pathologies in age-related disorders, creating a new opportunity for aging research. Generating therapies targeting the elimination of senescent cells would improve health span and increase longevity, making senolytics a promising therapy for cardiovascular diseases.
    Keywords:  Vascular aging; cardiovascular disease; endothelial dysfunction; senescence; senolytics
    DOI:  https://doi.org/10.20517/jca.2023.45
  3. Aging Cell. 2024 Aug 07. e14300
    Are immunosenescent T cells really senescent?
    Helena Slaets, Naomi Veeningen, Peter L J de Keizer, Niels Hellings, Sven Hendrix.
      Loss of proper T-cell functioning is a feature of aging that increases the risk of developing chronic diseases. In aged individuals, highly differentiated T cells arise with a reduced expression of CD28 and CD27 and an increased expression of KLRG-1 or CD57. These cells are often referred to as immunosenescent T cells but may still be highly active and contribute to autoimmunity. Another population of T cells known as exhausted T cells arises after chronic antigen stimulation and loses its effector functions, leading to a failure to combat malignancies and viral infections. A process called cellular senescence also increases during aging, and targeting this process has proven to be fruitful against a range of age-related pathologies in animal models. Cellular senescence occurs in cells that are irreparably damaged, limiting their proliferation and typically leading to chronic secretion of pro-inflammatory factors. To develop therapies against pathologies caused by defective T-cell function, it is important to understand the differences and similarities between immunosenescence and cellular senescence. Here, we review the hallmarks of cellular senescence versus senescent and exhausted T cells and provide considerations for the development of specific therapies against age-related diseases.
    Keywords:  T‐cells; exhaustion‐T‐lymphocytes; immunosenescence‐aging; senescence
    DOI:  https://doi.org/10.1111/acel.14300
  4. Neural Regen Res. 2024 Jul 29.
    Decoding molecular mechanisms: brain aging and Alzheimer's disease.
    Mahnoor Hayat, Rafay Ali Syed, Hammad Qaiser, Mohammad Uzair, Khalid Al-Regaiey, Roaa Khallaf, Lubna Abdullah Mohammed Albassam, Imdad Kaleem, Wang Xueyi, Wang Ran, Mehwish S Bhatti, Shahid Bashir.
      The complex morphological, anatomical, physiological, and chemical mechanisms within the aging brain have been the hot topic of research for centuries. The aging process alters the brain structure that affects functions and cognitions, but the worsening of such processes contributes to the pathogenesis of neurodegenerative disorders, such as Alzheimer's disease. Beyond these observable, mild morphological shifts, significant functional modifications in neurotransmission and neuronal activity exert a crucial influence on the aging brain. Understanding these changes is important for maintaining cognitive health, especially given the increasing prevalence of age-related conditions that affect cognition. This review aims to explore the age-induced changes in brain plasticity and molecular processes, differentiating normal aging from the pathogenesis of Alzheimer's disease thereby providing insights into predicting the risk of dementia, particularly Alzheimer's disease.
    DOI:  https://doi.org/10.4103/NRR.NRR-D-23-01403
  5. FEBS Lett. 2024 Aug 07.
    Oxidative stress and aging: synergies for age related diseases.
    ALFA Score Consortium
      Aging is characterized by a progressive decline in physiological function and underlies several disabilities, including the increased sensitivity of cells and tissues to undergo pathological oxidative stress. In recent years, efforts have been made to better understand the relationship between age and oxidative stress and further develop therapeutic strategies to minimize the impact of both events on age-related diseases. In this work, we review the impact of the oxidant and antioxidant systems during aging and disease development and discuss the crosstalk of oxidative stress and other aging processes, with a focus on studies conducted in elderly populations.
    Keywords:  healthy aging; oxidative modifications; oxidative stress
    DOI:  https://doi.org/10.1002/1873-3468.14995
  6. Bone Res. 2024 Aug 05. 12(1): 42
    Ageing-related bone and immunity changes: insights into the complex interplay between the skeleton and the immune system.
    Bobin Mi, Yuan Xiong, Samuel Knoedler, Michael Alfertshofer, Adriana C Panayi, Haixing Wang, Sien Lin, Gang Li, Guohui Liu.
      Ageing as a natural irreversible process inherently results in the functional deterioration of numerous organ systems and tissues, including the skeletal and immune systems. Recent studies have elucidated the intricate bidirectional interactions between these two systems. In this review, we provide a comprehensive synthesis of molecular mechanisms of cell ageing. We further discuss how age-related skeletal changes influence the immune system and the consequent impact of immune system alterations on the skeletal system. Finally, we highlight the clinical implications of these findings and propose potential strategies to promote healthy ageing and reduce pathologic deterioration of both the skeletal and immune systems.
    DOI:  https://doi.org/10.1038/s41413-024-00346-4
  7. Front Pharmacol. 2024 ;15 1413853
    Implications of endoplasmic reticulum stress and autophagy in aging and cardiovascular diseases.
    Chenguang Ma, Yang Liu, Zhiling Fu.
      The average lifespan of humans has been increasing, resulting in a rapidly rising percentage of older individuals and high morbidity of aging-associated diseases, especially cardiovascular diseases (CVDs). Diverse intracellular and extracellular factors that interrupt homeostatic functions in the endoplasmic reticulum (ER) induce ER stress. Cells employ a dynamic signaling pathway of unfolded protein response (UPR) to buffer ER stress. Recent studies have demonstrated that ER stress triggers various cellular processes associated with aging and many aging-associated diseases, including CVDs. Autophagy is a conserved process involving lysosomal degradation and recycling of cytoplasmic components, proteins, organelles, and pathogens that invade the cytoplasm. Autophagy is vital for combating the adverse influence of aging on the heart. The present report summarizes recent studies on the mechanism of ER stress and autophagy and their overlap in aging and on CVD pathogenesis in the context of aging. It also discusses possible therapeutic interventions targeting ER stress and autophagy that might delay aging and prevent or treat CVDs.
    Keywords:  ER stress; UPR; aging; autophagy; cardiovascular diseases
    DOI:  https://doi.org/10.3389/fphar.2024.1413853
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