bims-agimec Biomed News
on Aging mechanisms
Issue of 2025–03–09
nine papers selected by
Metin Sökmen, Ankara Üniversitesi
  1. Microplastics/nanoplastics contribute to aging and age-related diseases: Mitochondrial dysfunction as a crucial role.
  2. Mitochondrial Dysfunction in Alzheimer's Disease.
  3. The relationship between telomere length and aging-related diseases.
  4. Connecting the dots: Mitochondrial transfer in immunity, inflammation, and cancer.
  5. Engineered mitochondria in diseases: mechanisms, strategies, and applications.
  6. The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.
  7. Exploring the potential of stem cell therapy: Applications, types, and future directions.
  8. Cognitive resilience in Alzheimer's disease: Mechanism and potential clinical intervention.
  9. Anti-senescence therapies: a new concept to address cardiovascular disease.
  1. Food Chem Toxicol. 2025 Feb 26. pii: S0278-6915(25)00122-X. [Epub ahead of print]199 115355
    Microplastics/nanoplastics contribute to aging and age-related diseases: Mitochondrial dysfunction as a crucial role.
    Liang Kong, Shuhao Li, Yu Fu, Qinyun Cai, Zhengyu Zhai, Jingyan Liang, Tan Ma.
      The pervasive utilization of plastic products has led to a significant escalation in plastic waste accumulation. Concurrently, the implications of emerging pollutants such as microplastics (MPs) and nanoplastics (NPs) on human health are increasingly being acknowledged. Recent research has demonstrated that MPs/NPs may contribute to the onset of human aging and age-related diseases. Additionally, MPs/NPs have the potential to induce mitochondrial damage, resulting in mitochondrial dysfunction. Mitochondrial dysfunction is widely recognized as a hallmark of aging; thus, it is necessary to elucidate the relationship between them. In this article, we first elucidate the distribution of MPs/NPs in various environmental media, their pathways into the human body, and their subsequent distribution within human tissues and organs. Subsequently, we examine the interplay between MPs/NPs, mitochondrial dysfunction, and the aging process. We aspire that this article will enhance awareness regarding the toxicity of MPs/NPs while also offering a theoretical framework to support the development of improved regulatory policies in the future.
    Keywords:  Aging; MPs; Mitochondrial dysfunction; NPs
    DOI:  https://doi.org/10.1016/j.fct.2025.115355
  2. Ageing Res Rev. 2025 Feb 27. pii: S1568-1637(25)00059-5. [Epub ahead of print] 102713
    Mitochondrial Dysfunction in Alzheimer's Disease.
    Maria Clara Bila D'alessandro, Salim Kanaan, Mauro Geller, Domenico Praticò, João Paulo Lima Daher.
      Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by progressive cognitive decline and distinct neuropathological features. The absence of a definitive cure presents a significant challenge in neurology and neuroscience. Early clinical manifestations, such as memory retrieval deficits and apathy, underscore the need for a deeper understanding of the disease's underlying mechanisms. While amyloid-β plaques and tau neurofibrillary tangles have dominated research efforts, accumulating evidence highlights mitochondrial dysfunction as a central factor in AD pathogenesis. Mitochondria, essential cellular organelles responsible for energy production necessary for neuronal function become impaired in AD, triggering several cellular consequences. Factors such as oxidative stress, disturbances in energy metabolism, failures in the mitochondrial quality control system, and dysregulation of calcium release are associated with mitochondrial dysfunction. These abnormalities are closely linked to the neurodegenerative processes driving AD development and progression. This review explores the intricate relationship between mitochondrial dysfunction and AD pathogenesis, emphasizing its role in disease onset and progression, while also considering its potential as a biomarker and a therapeutic target.
    Keywords:  Mitochondrial dysfunction. Alzheimer’ disease. Pathology. Mitophagy. Neurodegeneration
    DOI:  https://doi.org/10.1016/j.arr.2025.102713
  3. Clin Exp Med. 2025 Mar 05. 25(1): 72
    The relationship between telomere length and aging-related diseases.
    Xuanqi Huang, Leyi Huang, Jiaweng Lu, Lijuan Cheng, Du Wu, Linmeng Li, Shuting Zhang, Xinyue Lai, Lu Xu.
      The intensifying global phenomenon of an aging population has spurred a heightened emphasis on studies on aging and disorders associated with aging. Cellular senescence and aging are known to be caused by telomere shortening. Telomere length (TL) has emerged as a biomarker under intense scrutiny, and its widespread use in investigations of diseases tied to advancing age. This review summarizes the current knowledge of the association between telomeres and aging-related diseases, explores the important contribution of dysfunctional telomeres to the development and progression of these diseases, and aims to provide valuable insights for the development of novel therapeutic strategies.
    Keywords:  Aging-related diseases; Biomarkers; Telomere length
    DOI:  https://doi.org/10.1007/s10238-025-01608-z
  4. Immunol Lett. 2025 Mar 06. pii: S0165-2478(25)00024-0. [Epub ahead of print]274 106992
    Connecting the dots: Mitochondrial transfer in immunity, inflammation, and cancer.
    Valentina Artusa, Lara De Luca, Mario Clerici, Daria Trabattoni.
      Mitochondria are more than mere energy generators; they are multifaceted organelles that integrate metabolic, signalling, and immune functions, making them indispensable players in maintaining cellular and systemic health. Mitochondrial transfer has recently garnered attention due to its potential role in several physiological and pathological processes. This process involves multiple mechanisms by which mitochondria, along with mitochondrial DNA and other components, are exchanged between cells. In this review, we examine the critical roles of mitochondrial transfer in health and disease, focusing on its impact on immune cell function, the resolution of inflammation, tissue repair, and regeneration. Additionally, we explore its implications in viral infections and cancer progression. We also provide insights into emerging therapeutic applications, emphasizing its potential to address unmet clinical needs.
    Keywords:  Cancer; Immunity; Inflammation; Mitochondrial transfer; Mitotherapy
    DOI:  https://doi.org/10.1016/j.imlet.2025.106992
  5. Signal Transduct Target Ther. 2025 Mar 03. 10(1): 71
    Engineered mitochondria in diseases: mechanisms, strategies, and applications.
    Mingyang Li, Limin Wu, Haibo Si, Yuangang Wu, Yuan Liu, Yi Zeng, Bin Shen.
      Mitochondrial diseases represent one of the most prevalent and debilitating categories of hereditary disorders, characterized by significant genetic, biological, and clinical heterogeneity, which has driven the development of the field of engineered mitochondria. With the growing recognition of the pathogenic role of damaged mitochondria in aging, oxidative disorders, inflammatory diseases, and cancer, the application of engineered mitochondria has expanded to those non-hereditary contexts (sometimes referred to as mitochondria-related diseases). Due to their unique non-eukaryotic origins and endosymbiotic relationship, mitochondria are considered highly suitable for gene editing and intercellular transplantation, and remarkable progress has been achieved in two promising therapeutic strategies-mitochondrial gene editing and artificial mitochondrial transfer (collectively referred to as engineered mitochondria in this review) over the past two decades. Here, we provide a comprehensive review of the mechanisms and recent advancements in the development of engineered mitochondria for therapeutic applications, alongside a concise summary of potential clinical implications and supporting evidence from preclinical and clinical studies. Additionally, an emerging and potentially feasible approach involves ex vivo mitochondrial editing, followed by selection and transplantation, which holds the potential to overcome limitations such as reduced in vivo operability and the introduction of allogeneic mitochondrial heterogeneity, thereby broadening the applicability of engineered mitochondria.
    DOI:  https://doi.org/10.1038/s41392-024-02081-y
  6. Research (Wash D C). 2025 ;8 0612
    The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.
    Jie Wang, Fanglin Shao, Qing Xin Yu, Luxia Ye, Dilinaer Wusiman, Ruicheng Wu, Zhouting Tuo, Zhipeng Wang, Dengxiong Li, William C Cho, Wuran Wei, Dechao Feng.
      The intricate relationship between cancer, circadian rhythms, and aging is increasingly recognized as a critical factor in understanding the mechanisms underlying tumorigenesis and cancer progression. Aging is a well-established primary risk factor for cancer, while disruptions in circadian rhythms are intricately associated with the tumorigenesis and progression of various tumors. Moreover, aging itself disrupts circadian rhythms, leading to physiological changes that may accelerate cancer development. Despite these connections, the specific interplay between these processes and their collective impact on cancer remains inadequately explored in the literature. In this review, we systematically explore the physiological mechanisms of circadian rhythms and their influence on cancer development. We discuss how core circadian genes impact tumor risk and prognosis, highlighting the shared hallmarks of cancer and aging such as genomic instability, cellular senescence, and chronic inflammation. Furthermore, we examine the interplay between circadian rhythms and aging, focusing on how this crosstalk contributes to tumorigenesis, tumor proliferation, and apoptosis, as well as the impact on cellular metabolism and genomic stability. By elucidating the common pathways linking aging, circadian rhythms, and cancer, this review provides new insights into the pathophysiology of cancer and identifies potential therapeutic strategies. We propose that targeting the circadian regulation of cancer hallmarks could pave the way for novel treatments, including chronotherapy and antiaging interventions, which may offer important benefits in the clinical management of cancer.
    DOI:  https://doi.org/10.34133/research.0612
  7. Acta Histochem. 2025 Feb 27. pii: S0065-1281(25)00009-1. [Epub ahead of print]127(2): 152237
    Exploring the potential of stem cell therapy: Applications, types, and future directions.
    KeerthiShri Boopathy, Thirunavukkarasu Palaniyandi, Maddaly Ravi, Mugip Rahaman Abdul Wahab, Gomathy Baskar, Safia Obaidur Rab, Mohd Saeed, Vishal M Balaramnavar.
      One of the most significant treatment approaches now accessible is stem cell therapy. Over the last few decades, a lot of study has been done in this field, and this fascinating feature of plasticity could have therapeutic uses. The potential of stem cells to restore function lost as a result of disease, trauma, congenital defects, and age has made stem cell research a key priority for scientific and medical organizations across the world. Stem cells are a crucial topic of study in regenerative medicine because of their capacity to replace, repair, or regenerate damaged cells, tissues, or organs. As a result, stem cell therapy is being used as a treatment strategy for a number of illnesses. Because stem cells may proliferate indefinitely and generate vast quantities of differentiated cells needed for transplantation, they hold enormous promise for regenerative medicine. Stem cells can be reprogrammed from adult cell types or originate from embryonic or fetal origins. Depending on their availability and place of origin, stem cells can be totipotent, pluripotent, multipotent, oligopotent, or unipotent. With stem cell treatment, many ailments, including diabetes, liver disease, infertility, wounds and traumas, neurological disorders, cardiovascular disease, and cancer, might be cured. Various types of stem cell treatment are described in this review along with their applications in different therapeutic fields, ethical considerations, and advantages and disadvantages.
    Keywords:  Differentiation; Regenerative therapy; Stem cell therapy; Stem cells; Transplantation
    DOI:  https://doi.org/10.1016/j.acthis.2025.152237
  8. Ageing Res Rev. 2025 Feb 26. pii: S1568-1637(25)00057-1. [Epub ahead of print]106 102711
    Cognitive resilience in Alzheimer's disease: Mechanism and potential clinical intervention.
    Bin Jia, Yun Xu, Xiaolei Zhu.
      Alzheimer's disease (AD) is a globally recognized neurodegenerative disorder that severely impairs cognitive function and imposes substantial psychological and financial burdens on patients and their families. The hallmark pathological features of AD include progressive neurodegeneration, extracellular beta-amyloid (Aβ) plaque accumulation, and intracellular hyperphosphorylated tau protein tangles. However, recent studies have identified a subset of patients exhibiting cognitive resilience, characterized by a slower cognitive decline or the preservation of high cognitive function despite the presence of AD pathology. Cognitive resilience is influenced by a complex interplay of genetic, environmental, and lifestyle factors. In addition, cognitive resilience contributes to the new perspectives on the diagnosis and personalized treatment of AD. This review aims to provide a comprehensive analysis of current studies on cognitive resilience in AD and to explore future research directions of AD diagnosis and treatment.
    Keywords:  Alzheimer's disease; Diagnosis; Pathology; Personalized intervention strategies; Resilience
    DOI:  https://doi.org/10.1016/j.arr.2025.102711
  9. Cardiovasc Res. 2025 Feb 28. pii: cvaf030. [Epub ahead of print]
    Anti-senescence therapies: a new concept to address cardiovascular disease.
    Stevan D Stojanović, Thomas Thum, Johann Bauersachs.
      Accumulation of senescent cells is an increasingly recognized factor in the development and progression of cardiovascular disease. Senescent cells of different types display a pro-inflammatory and matrix remodeling molecular program, known as the 'senescence associated secretory phenotype' (SASP), which has roots in (epi)genetic changes. Multiple therapeutic options (senolytics, anti-SASP senomorphics and epigenetic reprogramming) that delete or ameliorate cellular senescence have recently emerged. Some drugs routinely used in the clinics also have anti-senescence effects. However, multiple challenges hinder the application of novel anti-senescence therapeutics in the clinical setting. Understanding the biology of cellular senescence, advantages and pitfalls of anti-senescence treatments, as well as patients that can profit from these interventions is necessary to introduce this novel therapeutic modality into the clinics. We provide a guide through the molecular machinery of senescent cells, systematize anti-senescence treatments and propose a pathway towards senescence-adapted clinical trial design to aid future efforts.
    DOI:  https://doi.org/10.1093/cvr/cvaf030
This page is being maintained by Thomas Krichel. It was last updated on 2025‒04‒28 at 12:28.