bims-agimec Biomed News
on Aging mechanisms
Issue of 2025–02–09
seven papers selected by
Metin Sökmen, Ankara Üniversitesi



  1. Biogerontology. 2025 Feb 07. 26(2): 58
      Aging is a complex and heterogeneous biological process characterized by telomere attrition, genomic instability, mitochondrial dysfunction, and disruption in nutrient sensing. Besides contributing to the progression of cancer, metabolic disorders, and neurodegenerative diseases, these manifestations of aging also adversely affect organ function. It is crucial to understand these mechanisms and identify interventions to modulate them to promote healthy aging and prevent age-related diseases. Vitamins have emerged as potential modulators of aging beyond their traditional roles in health maintenance. There is an increasing body of evidence that hormetic effects of vitamins are responsible for activating cellular stress responses, repair mechanisms, and homeostatic processes when mild stress is induced by certain vitamins. It is evident from this dual role that vitamins play a significant role in preventing frailty, promoting resilience, and mitigating age-related cellular damage. Moreover, addressing vitamin deficiencies in the elderly could have a significant impact on slowing aging and extending life expectancy. A review of recent advances in the role of vitamins in delaying aging processes and promoting multiorgan health is presented in this article. The purpose of this paper is to provide a comprehensive framework for using vitamins as strategic tools for fostering longevity and vitality. It offers a fresh perspective on vitamins' role in aging research by bridging biological mechanisms and clinical opportunities.
    Keywords:  Aging; Epigenetic; Immune system; Longevity; Oxidative stress; Vitamin
    DOI:  https://doi.org/10.1007/s10522-025-10202-5
  2. Geroscience. 2025 Feb 06.
      There is a growing interest in developing drugs with a general geroprotective effect, aimed at slowing down aging. Several compounds have been shown to increase the lifespan and reduce the incidence of age-related diseases in model organisms. Translating these results is challenging, due to the long lifespan of humans. To address this, we propose using a battery of medical imaging protocols that allow for assessments of age-related processes known to precede disease onset. These protocols, based on magnetic resonance imaging, positron emission-, computed-, and optical coherence tomography, are already in use in drug development and are available at most modern hospitals. Here, we outline how an informed use of these techniques allows for detecting changes in the accumulation of age-related pathologies in a diverse set of physiological systems. This in vivo imaging battery enables efficient screening of candidate geroprotective compounds in early phase clinical trials, within reasonable trial durations.
    Keywords:  Age-related disease; Biomarker; CT; Drug development; Geroprotection; Imaging; MRI; OCT; PET
    DOI:  https://doi.org/10.1007/s11357-025-01514-y
  3. Adv Biol (Weinh). 2025 Feb 06. e2400469
      SIRT6 is a NAD+-dependent histone deacetylase with crucial roles in controlling DNA damage repair, telomere homeostasis, oxidative stress, autophagy, and other cellular processes, and it has long been recognized as a longevity-associated protein. This review details its anti-aging-related mechanisms. First, SIRT6 facilitates DNA repair pathways and maintains genome stability by deacetylating histone H3 at K56, K9, and K18 residues, in addition to participating in DNA damage repair through mono-ADP-ribosylation and other mechanisms. Second, SIRT6 preserves telomere integrity and mitigates cellular senescence by reducing oxidative stress-induced damage through the regulation of reactive oxygen species (ROS), inhibition of inflammation, and other pathways. Furthermore, SIRT6 promotes autophagy, slowing cellular senescence via the modulation of various signaling pathways, including AMPK, IGF-Akt-mTOR, H133Y, IL-1β, and mitochondrial autophagy-related proteins. Finally, SIRT6 regulates multiple signaling pathways, such asNF-κB, FOXO, and AMPK, to counteract the aging process. This review particularly delves into the interplay between SIRT6 and various diseases, including tumors, cardiovascular diseases (e.g., atherosclerosis, heart failure), metabolic diseases (e.g., type 2 diabetes, dyslipidemia, gluconeogenesis, osteoporosis), and neurodegenerative diseases (e.g., Alzheimer's disease). Moreover, recent advancements in SIRT6-regulated compounds (e.g., C3G, BZBS, Fisetin, FNDC5, Lycorine hydrochloride, and Ergothioneine) are discussed as potential therapeutic agents for these mediated diseases.
    Keywords:  SIRT6; mechanisms of senescence; senescence; senescence‐related diseases; signaling pathway
    DOI:  https://doi.org/10.1002/adbi.202400469
  4. Curr Obes Rep. 2025 Feb 03. 14(1): 17
       PURPOSE OF REVIEW: In this review, we summarize the molecular effects of time-restricted eating (TRE) and its possible role in appetite regulation. We also discuss the potential clinical benefits of TRE in obesity.
    RECENT FINDINGS: TRE is an emerging dietary approach consisting in limiting food intake to a specific window of time each day. The rationale behind this strategy is to restore the circadian misalignment, commonly seen in obesity. Preclinical studies have shown that restricting food intake only during the active phase of the day can positively influence several cellular functions including senescence, mitochondrial activity, inflammation, autophagy and nutrients' sensing pathways. Furthermore, TRE may play a role by modulating appetite and satiety hormones, though further research is needed to clarify its exact mechanisms. Clinical trials involving patients with obesity or type 2 diabetes suggest that TRE can be effective for weight loss, but its broader effects on improving other clinical outcomes, such as cardiovascular risk factors, remain less certain. The epidemic proportions of obesity cause urgency to find dietary, pharmacological and surgical interventions that can be effective in the medium and long term. According to its molecular effects, TRE can be an interesting alternative to caloric restriction in the treatment of obesity, but the considerable variability across clinical trials regarding population, intervention, and follow-up duration makes it difficult to reach definitive conclusions.
    Keywords:  Appetite; Biological clock; Circadian rhythm; Obesity; Time restricted eating
    DOI:  https://doi.org/10.1007/s13679-025-00609-z
  5. MedComm (2020). 2025 Feb;6(2): e70079
      Circular RNA (circRNA), a subtype of noncoding RNA, has emerged as a significant focus in RNA research due to its distinctive covalently closed loop structure. CircRNAs play pivotal roles in diverse physiological and pathological processes, functioning through mechanisms such as miRNAs or proteins sponging, regulation of splicing and gene expression, and serving as translation templates, particularly in the context of various cancers. The hallmarks of cancer comprise functional capabilities acquired during carcinogenesis and tumor progression, providing a conceptual framework that elucidates the nature of the malignant transformation. Although numerous studies have elucidated the role of circRNAs in the hallmarks of cancers, their functions in the development of chemoradiotherapy resistance remain unexplored and the clinical applications of circRNA-based translational therapeutics are still in their infancy. This review provides a comprehensive overview of circRNAs, covering their biogenesis, unique characteristics, functions, and turnover mechanisms. We also summarize the involvement of circRNAs in cancer hallmarks and their clinical relevance as biomarkers and therapeutic targets, especially in thyroid cancer (TC). Considering the potential of circRNAs as biomarkers and the fascination of circRNA-based therapeutics, the "Ying-Yang" dynamic regulations of circRNAs in TC warrant vastly dedicated investigations.
    Keywords:  biomarker; circular RNA; hallmarks of cancer; therapeutic targets; thyroid cancer
    DOI:  https://doi.org/10.1002/mco2.70079
  6. Mol Biol Rep. 2025 Jan 31. 52(1): 183
      Alzheimer's disease is a progressive neurodegenerative disorder primarily affecting individuals aged 65 and older, characterized by cognitive decline and diminished quality of life. The molecular hallmarks of AD include extracellular β-amyloid plaques, intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein, and chronic neuroinflammation. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), have emerged as potential therapeutic targets due to their regulatory roles in AD pathogenesis. For example, miR-124 has been shown to modulate Aβ levels, while lncRNAs such as BACE1-AS regulate the expression of BACE1, a crucial enzyme in Aβ production. Transcriptomic studies of AD patients have revealed dysregulation of ncRNA expression, further supporting their involvement in disease progression. This review examines the regulatory functions of ncRNAs in AD, focusing on their impact on Aβ, tau hyperphosphorylation, and neuroinflammation. Additionally, we discuss the emerging role of ncRNAs in liquid-liquid phase separation and the formation of protein aggregates, key processes contributing to AD pathology.
    Keywords:  Alzheimer’s disease; Liquid–liquid phase separation; Tau protein; ncRNAs; β-amyloid
    DOI:  https://doi.org/10.1007/s11033-025-10284-x
  7. NPJ Biol Phys Mech. 2025 ;2(1): 3
      The cancer metastatic cascade includes a series of mechanical barrier-crossing events, involving the physical movement of cancer cells from their primary location to a distant organ. This review describes the physical changes that influence tumour proliferation, progression, and metastasis. We identify potential mechanical signatures at every step of the metastatic cascade and discuss some latest mechanobiology-based therapeutic interventions to highlight the importance of interdisciplinary approaches in cancer diagnosis and treatment.
    Keywords:  Biological physics; Diseases
    DOI:  https://doi.org/10.1038/s44341-024-00007-x