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As the global population continues to age, the prevalence of age-related diseases is increasing, significantly influencing social and economic development, the stability of social security systems, and progress in medical technology. Ferroptosis, a recently discovered form of programmed cell death driven by iron-dependent lipid peroxidation, has emerged as a key area of research. Studies have revealed a strong association between ferroptosis and senescence. In this article, we systematically summarize the molecular mechanisms and associated signaling pathways underlying ferroptosis, emphasizing its pivotal role in the onset and progression of age-related diseases. By providing new perspectives, we aim to advance understanding of the pathogenesis of age-related diseases and guide the development of effective intervention strategies. [ABSTRACT FROM AUTHOR]

Background: The amount of physical activity, sleep, and sedentary behaviour affect several age-related diseases. However, no relevant study about their associations with cardiovascular and musculoskeletal diseases from European older adults is known. Methods: We investigated the associations of the volumes of physical activity, sleep, and sedentary behaviour with low handgrip strength (HGS), heart attack, hip fracture, rheumatoid arthritis, stroke, and osteoarthritis among European older adults (age ≥ 50 years, n = 819) from ten countries using cross-sectional data from the Survey of Health, Ageing, and Retirement in Europe (SHARE) conducted between 2019 and 2021. We used iso-temporal regression analysis to investigate the associations of lifestyle factors with age-related diseases. Results: The participants who met the weekly recommendation for 150 min of moderate-to-vigorous physical activity (MVPA) had lower prevalence of low HGS, difficulty lifting 5 kg of weight, heart attack, hip fracture, rheumatoid arthritis, stroke, and osteoarthritis. The iso-temporal regression analysis revealed that more light physical activity or MVPA was associated with lower prevalence of difficulty lifting 5 kg of weight and stroke. Lastly, longer sleep or less MVPA was associated with higher prevalence of stroke and difficulty lifting 5 kg of weight. Conclusions: Collectively, our data shows the associations of several age-related diseases and optimal LPA, MVPA, and an optimal sleep. Our observations may be useful in optimizing lifestyle to combat age-related disorders in European older adults. [ABSTRACT FROM AUTHOR]

Aging and age-related disease are among the most common and challenging issues worldwide. During the aging process, the accumulation of oxidative stress, DNA damage, telomere dysfunction, and other related changes lead to cellular dysfunction and the development of diseases such as neurodegenerative and cardiovascular conditions. Curcumin is a widely-used dietary supplement against various diseases such as cancer, diabetes, cardiovascular diseases and aging. This agent mediates its effects through several mechanisms, including the reduction of reactive oxygen species (ROS) and oxidative stress-induced damage, as well as the modulation of subcellular signaling pathways such as AMPK, AKT/mTOR, and NF-κB. These pathways are involved in cellular senescence and inflammation, and their modulation can improve cell function and help prevent disease. In cancer, Curcumin can induce apoptosis in a variety of different tumor cell lines. Curcumin also activates redox reactions within cells inducing ROS production that leads to the upregulation of apoptosis receptors on the tumor cell membrane. Curcumin can also upregulate the expression and activity of p53 that inhibits tumor cell proliferation and increases apoptosis. Furthermore, curcumin has a potent inhibitory effect on the activity of nuclear factor kappa B (NF-κB) and cyclooxygenase-2 (COX-2) , which are involved in the overexpression of antiapoptosis genes such as Bcl-2. It can also attenuate the regulation of antiapoptosis phosphoinositide 3-kinases (PI3K) signaling and increase the expression of mitogen-activated protein kinases (MAPKs) to induce endogenous production of ROS. Therefore, herein, we aim to summarize how curcumin affect different epigenetic processes (such as apoptosis and oxidative stress) in order to change aging-related mechanisms. Furthermore, we discuss its roles in age-related diseases, such as Alzheimer, Parkinson, osteoporosis, and cardiovascular diseases. [ABSTRACT FROM AUTHOR]

T cells play a critical and irreplaceable role in maintaining overall health. However, their functions undergo alterations as individuals age. It is of utmost importance to comprehend the specific characteristics of T-cell aging, as this knowledge is crucial for gaining deeper insights into the pathogenesis of aging-related diseases and developing effective therapeutic strategies. In this review, we have thoroughly examined the existing studies on the characteristics of immune organ aging. Furthermore, we elucidated the changes and potential mechanisms that occur in T cells during the aging process. Additionally, we have discussed the latest research advancements pertaining to T-cell aging-related diseases. These findings provide a fresh perspective for the study of T cells in the context of aging. [ABSTRACT FROM AUTHOR]

Simple Summary: Telomeres play an integral role in preventing genomic instability by protecting chromosomal ends using telomeric repeats, and their dysfunction may lead to premature aging disorders and age-related diseases. During cellular division, they undergo telomere attrition, resulting in the gradual shortening of those protective caps, leading to genomic instability and cellular aging. Critically short telomeres in normal cells trigger senescence, a major contributor to age-related diseases, and opens the door for genomic instability, which promotes carcinogenesis. This review aims to provide an updated overview of telomere biology and therapeutic strategies around telomere attrition. We emphasize the importance of understanding the complex balance between preserving telomere length in aging while inhibiting telomere maintenance in cancer by proposing Optimal Therapeutic Approaches based on the most updated literature. Background/Objectives: As cells divide, telomeres shorten through a phenomenon known as telomere attrition, which leads to unavoidable senescence of cells. Unprotected DNA exponentially increases the odds of mutations, which can evolve into premature aging disorders and tumorigenesis. There has been growing academic and clinical interest in exploring this duality and developing optimal therapeutic strategies to combat telomere attrition in aging and cellular immortality in cancer. The purpose of this review is to provide an updated overview of telomere biology and therapeutic tactics to address aging and cancer. Methods: We used the Rayyan platform to review the PubMed database and examined the ClinicalTrial.gov registry to gain insight into clinical trials and their results. Results: Cancer cells activate telomerase or utilize alternative lengthening of telomeres to escape telomere shortening, leading to near immortality. Contrarily, normal cells experience telomeric erosion, contributing to premature aging disorders, such as Werner syndrome and Hutchinson–Gilford Progeria, and (2) aging-related diseases, such as neurodegenerative and cardiovascular diseases. Conclusions: The literature presents several promising therapeutic approaches to potentially balance telomere maintenance in aging and shortening in cancer. This review highlights gaps in knowledge and points to the potential of these optimal interventions in preclinical and clinical studies to inform future research in cancer and aging. [ABSTRACT FROM AUTHOR]

Age-induced alterations in human immunity are often considered deleterious and are referred to as immunosenescence. The immune system monitors the number of senescent cells in the body, while immunosenescence may represent the initiation of systemic aging. Immune cells, particularly T cells, are the most impacted and involved in age-related immune function deterioration, making older individuals more prone to different age-related diseases. T-cell senescence can impact the effectiveness of immunotherapies that rely on the immune system's function, including vaccines and adoptive T-cell therapies. The research and practice of using senescent T cells as therapeutic targets to intervene in age-related diseases are in their nascent stages. Therefore, in this review, we summarize recent related literature to investigate the characteristics of senescent T cells as well as their formation mechanisms, relationship with various aging-related diseases, and means of intervention. The primary objective of this article is to explore the prospects and possibilities of therapeutically targeting senescent T cells, serving as a valuable resource for the development of immunotherapy and treatment of age-related diseases. [ABSTRACT FROM AUTHOR]

Aging is an inevitable biological process, and emerging research has highlighted the potential of dietary and pharmacological interventions to decelerate the trajectory of age-related diseases and prolong the health span. This study evaluates the protective effects of Musa balbisiana seed on healthy aging using D-galactose-induced accelerated aging rats. The results suggested that the bioactive ethyl acetate fraction of Musa balbisiana seed extract (BF) exhibited protective effects against aging-induced oxidative stress by reducing oxidative DNA damage, advanced glycation end-product formation, and malondialdehyde levels while restoring antioxidant and glyoxalase enzyme activities. BF also ameliorated neurodegeneration by decreasing acetylcholinesterase enzyme activity and amyloid beta plaque formation. Histopathological analysis demonstrated the protective effects of BF against brain aging, liver disruption, renal damage, and intestinal barrier dysfunction. BF further restored intestinal permeability by upregulating the tight junctions (zonula occludens 1 and 2, claudin 1,2,3 and 4, and occludin) and mucin (mucin 2 and mucin 5ac) gene expression while downregulating the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α). BF significantly induced the phosphorylation of FoxO3a proteins and upregulated the gene expression of SIRT1, PGC-1α, and TFAM in the hippocampus. Next-generation sequencing (NGS) of 16s rRNA amplicons of fecal metagenomics DNA and metabolites profiling showed that BF intervention restructured the gut microbiota and altered core metabolites related to cholesterol metabolism. Overall, our findings demonstrated the multifaceted protective effects of Musa balbisiana seed against D-galactose-induced aging. [Display omitted] • Musa balbisiana (MB) seed recovered aging-induced body weight loss. • Aging reduces antioxidant enzyme function, impacting oxidative stress management. • MB seed downregulates inflammatory cytokines in brain and intestine of aged rats. • MB seed restores intestinal barrier dysfunction and cognitive impairment. • MB seed restructures gut microbiota and metabolites differently from aged rats. [ABSTRACT FROM AUTHOR]

Abstract Background The amount of physical activity, sleep, and sedentary behaviour affect several age-related diseases. However, no relevant study about their associations with cardiovascular and musculoskeletal diseases from European older adults is known. Methods We investigated the associations of the volumes of physical activity, sleep, and sedentary behaviour with low handgrip strength (HGS), heart attack, hip fracture, rheumatoid arthritis, stroke, and osteoarthritis among European older adults (age ≥ 50 years, n = 819) from ten countries using cross-sectional data from the Survey of Health, Ageing, and Retirement in Europe (SHARE) conducted between 2019 and 2021. We used iso-temporal regression analysis to investigate the associations of lifestyle factors with age-related diseases. Results The participants who met the weekly recommendation for 150 min of moderate-to-vigorous physical activity (MVPA) had lower prevalence of low HGS, difficulty lifting 5 kg of weight, heart attack, hip fracture, rheumatoid arthritis, stroke, and osteoarthritis. The iso-temporal regression analysis revealed that more light physical activity or MVPA was associated with lower prevalence of difficulty lifting 5 kg of weight and stroke. Lastly, longer sleep or less MVPA was associated with higher prevalence of stroke and difficulty lifting 5 kg of weight. Conclusions Collectively, our data shows the associations of several age-related diseases and optimal LPA, MVPA, and an optimal sleep. Our observations may be useful in optimizing lifestyle to combat age-related disorders in European older adults.

Aging and age-related disease are among the most common and challenging issues worldwide. During the aging process, the accumulation of oxidative stress, DNA damage, telomere dysfunction, and other related changes lead to cellular dysfunction and the development of diseases such as neurodegenerative and cardiovascular conditions. Curcumin is a widely-used dietary supplement against various diseases such as cancer, diabetes, cardiovascular diseases and aging. This agent mediates its effects through several mechanisms, including the reduction of reactive oxygen species (ROS) and oxidative stress-induced damage, as well as the modulation of subcellular signaling pathways such as AMPK, AKT/mTOR, and NF-κB. These pathways are involved in cellular senescence and inflammation, and their modulation can improve cell function and help prevent disease. In cancer, Curcumin can induce apoptosis in a variety of different tumor cell lines. Curcumin also activates redox reactions within cells inducing ROS production that leads to the upregulation of apoptosis receptors on the tumor cell membrane. Curcumin can also upregulate the expression and activity of p53 that inhibits tumor cell proliferation and increases apoptosis. Furthermore, curcumin has a potent inhibitory effect on the activity of nuclear factor kappa B (NF-κB) and cyclooxygenase-2 (COX-2), which are involved in the overexpression of antiapoptosis genes such as Bcl-2. It can also attenuate the regulation of antiapoptosis phosphoinositide 3-kinases (PI3K) signaling and increase the expression of mitogen-activated protein kinases (MAPKs) to induce endogenous production of ROS. Therefore, herein, we aim to summarize how curcumin affect different epigenetic processes (such as apoptosis and oxidative stress) in order to change aging-related mechanisms. Furthermore, we discuss its roles in age-related diseases, such as Alzheimer, Parkinson, osteoporosis, and cardiovascular diseases.

The physiopathology of sarcopenia shares common biological cascades with the aging process, as does any other age-related condition. However, our understanding of the interconnected pathways between diagnosed sarcopenia and aging remains limited, lacking sufficient scientific evidence. This narrative review aims to gather and describe the current evidence on the relationship between biological aging determinants, commonly referred to as the hallmarks of aging, and diagnosed sarcopenia in humans. Among the twelve hallmarks of aging studied, there appears to be a substantial association between sarcopenia and mitochondrial dysfunction, epigenetic alterations, deregulated nutrient sensing, and altered intercellular communication. Although limited, preliminary evidence suggests a promising association between sarcopenia and genomic instability or stem cell exhaustion. Overall, an imbalance in energy regulation, characterized by impaired mitochondrial energy production and alterations in circulatory markers, is commonly associated with sarcopenia and may reflect the interplay between aging physiology and sarcopenia biology. • Sarcopenia, a prevalent age-related muscle disease, is linked to adverse outcomes. • Common biological pathways between aging and sarcopenia aren't fully understood yet. • The Hallmarks of Aging help elucidate aspects of sarcopenia physiopathology. • Energy imbalance and mitochondria dysfunction are signature features of sarcopenia. [ABSTRACT FROM AUTHOR]

As the global population continues to age, understanding the complex role of cellular senescence and its implications in healthy lifespans has gained increasing prominence. Cellular senescence is defined as the irreversible cessation of cell proliferation, accompanied by the secretion of a range of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP), in response to various cellular stresses. While the accumulation of senescent cells has been strongly implicated in the aging process and the pathogenesis of age-related diseases owing to their pro-inflammatory properties, recent research has also highlighted their essential roles in processes such as tumour suppression, tissue development, and repair. This review provides a comprehensive examination of the dual nature of senescent cells, evaluating their deleterious contributions to chronic inflammation, tissue dysfunction, and disease, as well as their beneficial roles in maintaining physiological homeostasis. Additionally, we explored the therapeutic potential of senolytic agents designed to selectively eliminate detrimental senescent cells while considering the delicate balance between transient and beneficial senescence and the persistence of pathological senescence. A deeper understanding of these dynamics is critical to develop novel interventions aimed at mitigating age-related dysfunctions and enhancing healthy life expectancies., (© The Author(s) 2025. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.)

In recent times, there has been growing interest in understanding the factors contributing to prolonged and healthy lifespans observed in specific populations, tribes, or countries. Factors such as environmental and dietary play significant roles in shaping the ageing process and are often the focus of inquiries seeking to unravel the secrets behind longevity. Among these factors, diet emerges as a primary determinant, capable of either promoting or mitigating the onset of age-related diseases that impact the ageing trajectory. This review examines the impact of various diet types on ageing and age-related conditions, including cardiovascular disease, cancer, neurodegenerative disorders, and metabolic syndrome. Different dietary patterns, such as the Mediterranean diet, the Japanese diet, vegetarian and vegan diets, as well as low-carbohydrate and ketogenic diets, are evaluated for their potential effects on longevity and health span. Each diet type is characterized by distinct nutritional profiles, emphasizing specific food groups, macronutrient compositions, and bioactive components, which may exert diverse effects on ageing processes and disease risk. Additionally, dietary factors such as calorie restriction, intermittent fasting, and dietary supplementation are explored for their potential anti-ageing and disease-modifying effects. Understanding the influence of various diet types on ageing and age-related diseases can inform personalized dietary recommendations and lifestyle interventions aimed at promoting healthy aging and mitigating age-associated morbidities., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)