Ageing Research Reviews最新文献

{"title":"Crosstalk between kidney and bones: New perspective for modulating osteoporosis","authors":"Yan Duan ,&nbsp;Li-juan Zhao ,&nbsp;Yu-ting Lu ,&nbsp;Juan Li ,&nbsp;Shun-xiang Li","doi":"10.1016/j.arr.2025.102776","DOIUrl":"10.1016/j.arr.2025.102776","url":null,"abstract":"<div><div>Growing evidence indicates an interesting interplay between kidney and bone. The pathophysiological condition of the skeletal system is intricately associated with the normal functioning of the kidneys. This relationship is modulated by various factors, including calcium and phosphate, 1-α-hydroxylase, erythropoietin (EPO), klotho, fibroblast growth factor 23 (FGF23), bone morphogenetic protein-7 (BMP-7), and extracellular vesicles (EVs). These interactions are notably evident in conditions such as chronic kidney disease with bone mineral density (CKD-BMD), renal osteodystrophy (ROD), and osteoporosis (OP). Furthermore, innovative methodologies such as cell co-culture, organ-on-a-chip, single-cell sequencing, and spatial transcriptomics are highlighted as instrumental in advancing the study of inter-organ interactions. This review, grounded in the pathogenesis, diagnostic and therapeutic modalities, and pharmacological treatments of OP, synthesizes evidence from molecular biology to clinical perspectives. It aims to establish a foundation for the development of more complex and physiologically relevant in vitro models and to propose potential therapeutic strategies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102776"},"PeriodicalIF":12.5,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144089420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREM2 in cardiovascular diseases: Mechanisms and therapeutic perspectives","authors":"Wengen Zhu ,&nbsp;Yue Zhou ,&nbsp;Yufan Wang ,&nbsp;Linjuan Guo ,&nbsp;Chen Liu","doi":"10.1016/j.arr.2025.102774","DOIUrl":"10.1016/j.arr.2025.102774","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) are the leading cause of global mortality, with immune responses playing a central role in their pathogenesis. Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immune regulator in CVDs, influencing inflammation, lipid metabolism, and tissue repair. This review comprehensively examines TREM2's structure, function, and signaling pathways, highlighting its roles in atherosclerosis, myocardial infarction, hypertension, atrial fibrillation, and heart failure. In atherosclerosis, macrophages with high TREM2 expression (TREM2^hi macrophages) promote plaque progression in early stages but enhance plaque stability in advanced stages. In myocardial infarction, TREM2 modulates macrophage diversity and efferocytosis, aiding cardiac repair. TREM2 also plays a protective role in hypertensive heart disease by reducing inflammation and promoting tissue repair. Challenges in targeting TREM2 therapeutically include its context-dependent effects and complex signaling pathways. Future research should focus on elucidating TREM2's mechanisms in CVDs and developing stage-specific therapies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102774"},"PeriodicalIF":12.5,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immersive virtual reality for older adults: Challenges and solutions in basic research and clinical applications","authors":"Malika Schaumburg ,&nbsp;Ashar Imtiaz ,&nbsp;Ruojing Zhou ,&nbsp;Matthieu Bernard ,&nbsp;Thomas Wolbers ,&nbsp;Vladislava Segen","doi":"10.1016/j.arr.2025.102771","DOIUrl":"10.1016/j.arr.2025.102771","url":null,"abstract":"<div><div>Immersive virtual reality (IVR) offers significant potential for aging research, providing a controlled yet ecologically valid platform for studying cognitive, emotional, and motor processes, as well as supporting interventions and diagnostic assessments in older adults. However, its usability can be hindered by age-related sensory, motor, and cognitive changes, which may contribute to anxiety, disorientation, and reduced task engagement. In this narrative review, we examine the challenges older adults face with IVR and explore strategies to optimize its design for this population. These challenges include negative attitudes, sensory and motor limitations, and cognitive decline, all of which influence interaction with virtual environments. Based on these insights, we discuss design considerations such as self-paced interactions, simplified control mechanisms, task-relevant visual and auditory adjustments, and structured training protocols to enhance engagement. Additionally, we highlight strategies to minimize cognitive load and physical discomfort, supporting the development of IVR applications that are both effective and accessible for aging populations.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102771"},"PeriodicalIF":12.5,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of ferroptosis in heart failure: The role of the RAGE/TLR4-JNK1/2 pathway in cardiomyocyte ferroptosis and intervention strategies","authors":"Zeyu Zhang ,&nbsp;Zhihua Yang ,&nbsp;Shuai Wang ,&nbsp;Xianliang Wang ,&nbsp;Jingyuan Mao","doi":"10.1016/j.arr.2025.102770","DOIUrl":"10.1016/j.arr.2025.102770","url":null,"abstract":"<div><div>The ferroptosis of cardiomyocytes has been recognized as the core pathological mechanism of heart failure. During the evolution of cardiovascular diseases, the accumulation of angiotensin II and advanced glycation end products can lead to the excessive activation of the RAGE/TLR4-JNK1/2 pathway, which subsequently triggers ferritinophagy, clockophagy, and enhanced p53 activity, ultimately leading to cardiomyocyte ferroptosis. It is evident that deeply unraveling the specific mechanisms in this field and comprehensively evaluating potential drugs and therapeutic strategies targeting this pathway is crucial for improving the status of cardiomyocyte ferroptosis. However, our current understanding of this pathway's specific molecular biological mechanisms in the process of cardiomyocyte ferroptosis remains limited. In light of this, this paper first comprehensively reviews the historical context of ferroptosis research, compares the similarities and differences between ferroptosis and other standard modes of cell death, elucidates the core mechanisms of ferroptosis and its close connection with heart failure, aiming to establish a basic cognitive framework for readers on ferroptosis and its role in heart failure. Subsequently, the paper delves into the pivotal role of the RAGE/TLR4-JNK1/2 pathway in cardiomyocyte ferroptosis and its intricate molecular biological regulatory network. Furthermore, it systematically integrates various therapeutic approaches aimed at inhibiting RAGE, TLR4, and JNK1/2 activity to alleviate cardiomyocyte ferroptosis, encompassing RNA interference technology, gene knockout techniques, small molecule inhibitors, natural active ingredients, as well as traditional Chinese and Western medicines, with the ultimate goal of forging new avenues and strategies for the prevention and treatment of heart failure.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102770"},"PeriodicalIF":12.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sestrin2 is a central regulator of mitochondrial stress responses in disease and aging","authors":"Ivo F. Machado ,&nbsp;Carlos M. Palmeira ,&nbsp;Anabela P. Rolo","doi":"10.1016/j.arr.2025.102762","DOIUrl":"10.1016/j.arr.2025.102762","url":null,"abstract":"<div><div>Mitochondria supply most of the energy for cellular functions and coordinate numerous cellular pathways. Their dynamic nature allows them to adjust to stress and cellular metabolic demands, thus ensuring the preservation of cellular homeostasis. Loss of normal mitochondrial function compromises cell survival and has been implicated in the development of many diseases and in aging. Although exposure to continuous or severe stress has adverse effects on cells, mild mitochondrial stress enhances mitochondrial function and potentially extends health span through mitochondrial adaptive responses. Over the past few decades, sestrin2 (SESN2) has emerged as a pivotal regulator of stress responses. For instance, SESN2 responds to genotoxic, oxidative, and metabolic stress, promoting cellular defense against stress-associated damage. Here, we focus on recent findings that establish SESN2 as an orchestrator of mitochondrial stress adaptation, which is supported by its involvement in the integrated stress response, mitochondrial biogenesis, and mitophagy. Additionally, we discuss the integral role of SESN2 in mediating the health benefits of exercise as well as its impact on skeletal muscle, liver and heart injury, and aging.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102762"},"PeriodicalIF":12.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143904121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intercellular communication after myocardial infarction: Macrophage as the centerpiece","authors":"Ao-lin Li ,&nbsp;Kang-zheng Guo ,&nbsp;Le-rong Yu ,&nbsp;Jun Ge ,&nbsp;Wei Zhou ,&nbsp;Jun-ping Zhang","doi":"10.1016/j.arr.2025.102757","DOIUrl":"10.1016/j.arr.2025.102757","url":null,"abstract":"<div><div>Post-myocardial infarction (MI) injury, repair, and remodeling are complex biological events orchestrated by the heart and immune cell populations, with immune-inflammation at the core. Macrophages, as the main immune cell population active throughout the post-MI injury to repair processes, are the core of this “drama”. Recently, single-cell sequencing and other techniques have revealed the heterogeneity of macrophage origins and the complexity of macrophage subpopulation transformation and intercellular communication after MI. Defining the changes in macrophage subpopulation dynamics and macrophage-centered intercellular communication after MI may represent new targeted therapeutic strategies. It also helps to select the optimal time point for anti-inflammatory or pro-repair accurately. Therefore, in this review, we summarize the major macrophage subpopulations active at different times after MI and their functional characteristics based on gene expression profiles. Meanwhile, we summarize macrophage-centered intercellular communication, focusing on how macrophages interact with cardiomyocytes, neutrophils, fibroblasts, endothelial cells, and other cardiac cells. Together, these dominate the transition from inflammatory injury to fibrotic repair in the infarcted heart. We also focus on the regulatory potential of immune metabolism in macrophage subpopulation transformation and intercellular communication after MI, particularly providing new insights about lactylation. We conclude by emphasizing macrophage-centric targeting strategies and clinical translational potential, to provide ideas for the clinical treatment of MI.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102757"},"PeriodicalIF":12.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging","authors":"Rupa Lavarti ,&nbsp;Tatiana Alvarez-Diaz ,&nbsp;Kyarangelie Marti ,&nbsp;Parmita Kar ,&nbsp;Raghavan Pillai Raju","doi":"10.1016/j.arr.2025.102760","DOIUrl":"10.1016/j.arr.2025.102760","url":null,"abstract":"<div><div>Aging is characterized by a steady loss of physiological integrity, leading to impaired function and increased vulnerability to death. Cell senescence is a biological process that progresses with aging and is believed to be a key driver of age-related diseases. Senescence, a hallmark of aging, also demonstrates its beneficial physiological aspects as an anti-cancer, pro-regenerative, homeostatic, and developmental mechanism. A transitory response in which the senescent cells are quickly formed and cleared may promote tissue regeneration and organismal fitness. At the same time, senescence-related secretory phenotypes associated with extended senescence can have devastating effects. The fact that the interaction between senescent cells and their surroundings is very context-dependent may also help to explain this seemingly opposing pleiotropic function. Further, mitochondrial dysfunction is an often-unappreciated hallmark of cellular senescence and figures prominently in multiple feedback loops that induce and maintain the senescent phenotype. This review summarizes the mechanism of cellular senescence and the significance of acute senescence. We concisely introduced the context-dependent role of senescent cells and SASP, aspects of mitochondrial biology altered in the senescent cells, and their impact on the senescent phenotype. Finally, we conclude with recent therapeutic advancements targeting cellular senescence, focusing on acute injuries and age-associated diseases. Collectively, these insights provide a future roadmap for the role of senescence in organismal fitness and life span extension.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102760"},"PeriodicalIF":12.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of blood biomarkers with frailty–A mapping review","authors":"Lea Fritzenschaft ,&nbsp;Felix Boehm ,&nbsp;Dietrich Rothenbacher ,&nbsp;Michael Denkinger ,&nbsp;Dhayana Dallmeier","doi":"10.1016/j.arr.2025.102761","DOIUrl":"10.1016/j.arr.2025.102761","url":null,"abstract":"<div><div>Frailty describes a geriatric syndrome characterized by an increased vulnerability. Although a variety of potential blood-based biomarkers have been discussed for its characterization, a reliable protocol considering blood-based biomarkers for this purpose is still missing. However, a comprehensive overview on these biomarkers is necessary to understand potential molecular pathways to frailty. We, therefore, performed a mapping review to identify those blood-based biomarkers most consistently associated with frailty in community-dwelling older adults as well as possible analytical gaps according to the available literature. A proposed weighted correlation index (CI) describing the direction and consistency of the association considering the number of available publications as well as the size of the study populations was calculated for each biomarker. Overall, 72 manuscripts were critically reviewed reporting on a total of 82 biomarkers. The most consistent positive association with at least 3 articles addressing the respective biomarker in unadjusted and fully adjusted models was shown for interleukin 6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), neopterin, white blood cells count, glycated hemoglobin A1c (HbA1c) and sex hormone binding-globuline (SHBG) with a CI ≥ 0.7, while for negative association hemoglobin, 25-hydroxy vitamin D, free testosterone in men and albumin with a CI ≤ -0.7 were identified.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102761"},"PeriodicalIF":12.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethnicity and frailty: A systematic review of association with prevalence, incidence, trajectories and risks","authors":"Maryam Khan,&nbsp;Barbara I. Nicholl,&nbsp;Peter Hanlon","doi":"10.1016/j.arr.2025.102759","DOIUrl":"10.1016/j.arr.2025.102759","url":null,"abstract":"<div><h3>Background</h3><div>Ethnic variations in frailty are not fully understood. This systematic review examined ethnic differences in the prevalence, incidence and trajectories of frailty; associations between frailty and sociodemographic/lifestyle risk-factors; and health-related outcomes of frailty.</div></div><div><h3>Methods</h3><div>We searched four electronic databases from 2000 to July 2023 using terms for ethnicity and frailty. Inclusion criteria: observational studies assessing frailty in adults ≥ 18 years from community-based settings, including care homes; ethnicity defined by race, country of birth, language, ancestry, or culture. We supplemented searches with manual citation and reference list searches. Outcomes included prevalence, incidence, and transitions of frailty; factors associated with frailty; and health-related outcomes (e.g., mortality). Two reviewers independently screened all articles.</div></div><div><h3>Results</h3><div>We included 82 studies, representing data from 13 countries plus two multi-national samples. Across the included countries, frailty prevalence was higher in minority groups compared to majority groups. Ethnic differences appear sensitive to methods used to measure frailty. Two United States-based studies found that ethnic differences were independent of sociodemographic differences such as income or education. Six studies from the United States or United Kingdom showed that Black and South-Asian people, respectively, had higher frailty incidence or more rapid frailty progression. Two studies showed that frailty was associated with mortality across ethnic groups but with some small differences in magnitude between groups.</div></div><div><h3>Conclusion</h3><div>Ethnic disparities in frailty prevalence persist across community-based settings in different countries and are not fully explained by known inequalities. Addressing these disparities will likely require careful frailty measurement and assessment; confronting structural inequalities; and tailoring interventions to the needs of minoritised populations.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"109 ","pages":"Article 102759"},"PeriodicalIF":12.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143900038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid droplets: Emerging therapeutic targets for age-related metabolic diseases","authors":"Zheying Ma ,&nbsp;Shou Pan ,&nbsp;Yaming Yang ,&nbsp;Huiqian Ren ,&nbsp;Sikun Yin ,&nbsp;Qianyu Chen ,&nbsp;Zhenxian An ,&nbsp;Xiaoqin Zhao ,&nbsp;Zujie Xu","doi":"10.1016/j.arr.2025.102758","DOIUrl":"10.1016/j.arr.2025.102758","url":null,"abstract":"<div><div>Lipids metabolism is crucial in regulating aging and metabolic diseases. Lipid droplets (LDs) are dynamic, complex organelles responsible for the storage and release of neutral lipids, essential for maintaining lipid homeostasis and energy metabolism. Aging accelerates the accumulation of LDs, functional deterioration, and metabolic disorders, thereby inducing age-related metabolic diseases (ARMDs). This review examines published datasets on the association between LDs and ARMDs, focusing on the structure and function of LDs, their interactions with other organelles, and associated proteins. Furthermore, we explore the potential mechanisms by which LDs mediate the onset of ARMDs, including Alzheimer’s disease (AD), sarcopenia, metabolic cardiomyopathy, non-alcoholic fatty liver disease (NAFLD), and cancer. Lastly, we discuss intervention strategies aimed at targeting LDs to improve outcomes in ARMDs, including exercise, dietary, and pharmacological interventions.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102758"},"PeriodicalIF":12.5,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}