Ageing Research Reviews最新文献

{"title":"Decoding JMJD proteins in cardiovascular and cerebrovascular diseases: From structure to function","authors":"Guangzhi Hao ,&nbsp;Yiyang Chen ,&nbsp;Yong Liang ,&nbsp;Jiayan Li ,&nbsp;Yushu Dong ,&nbsp;Yang Yang","doi":"10.1016/j.arr.2025.102869","DOIUrl":"10.1016/j.arr.2025.102869","url":null,"abstract":"<div><div>Cardiovascular and cerebrovascular diseases remain major causes of death and disability worldwide. Their susceptibility is closely linked to epigenetic modifications triggered by environmental factors. The Jumonji C domain-containing (JMJD) protein family consists of Fe²⁺- and 2-oxoglutarate (2OG)-dependent oxidases that primarily mediate histone demethylation or hydroxylation of specific amino acid residues, functioning as critical histone demethylases in epigenetic regulation. Recent studies have identified JMJD proteins as pivotal epigenetic regulators in various cardiovascular and cerebrovascular diseases, including cardiac hypertrophy (CH), atherosclerosis (AS), myocardial ischemia-reperfusion injury (MIRI), and ischemic stroke (IS). These proteins are deeply involved in pathological processes such as oxidative stress, macrophage polarization, mitochondrial autophagy, and apoptosis. Accordingly, elucidating the functions of JMJD proteins has gained increasing attention. This review summarizes the structural characteristics of JMJD family members and highlights their roles in cardiovascular and cerebrovascular disorders. These insights may help guide future pharmacological strategies targeting JMJD proteins.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102869"},"PeriodicalIF":12.4,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144839336","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":"Application of Traditional Chinese Medicine in the different pathological stages of ischemic stroke: Target immune cells","authors":"Yulu Wang ,&nbsp;Yuanyi Wang ,&nbsp;Lele Liu ,&nbsp;Zhen Hui ,&nbsp;Sulei Wang ,&nbsp;Guoxue Zhu ,&nbsp;Lining Wang ,&nbsp;Zhennian Zhang ,&nbsp;Yue Hu","doi":"10.1016/j.arr.2025.102866","DOIUrl":"10.1016/j.arr.2025.102866","url":null,"abstract":"<div><div>Immune cells play a pivotal role in the complex pathophysiology of ischemic stroke (IS), with their functions dynamically shifting throughout the disease's progression. Throughout the different pathological stages of IS, various immune cells, such as microglia, T cells, neutrophils, NK cells, and mononuclear/macrophages, contribute uniquely to the disease's trajectory. Although thrombolytic therapy remains the standard treatment for IS, its efficacy is limited by a narrow therapeutic window, underscoring the need for alternative or adjunctive therapeutic strategies. Increasingly, the therapeutic potential of Traditional Chinese Medicine (TCM) has gained recognition for its beneficial effects across multiple phases of IS. Notably, TCM interventions have been shown to attenuate early inflammatory responses and neural injury by targeting immune cells, particularly microglia. Furthermore, during the recovery phase, TCM may promote white matter repair and functional recovery through the regulation of neuroimmune interactions. This review offers a comprehensive analysis of the dynamic roles and signaling pathways of immune cells in IS, and further investigates the mechanistic basis of TCM's immunomodulatory effects. While considerable progress has been made, significant challenges remain in fully elucidating the underlying mechanisms of TCM and in optimizing its integration into current IS treatment frameworks.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102866"},"PeriodicalIF":12.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818623","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":"Pathogens accelerate features of human aging: A review of molecular mechanisms","authors":"Amy D. Proal ,&nbsp;Michael B. VanElzakker","doi":"10.1016/j.arr.2025.102865","DOIUrl":"10.1016/j.arr.2025.102865","url":null,"abstract":"<div><div>Many models of aging assume that processes such as cellular senescence or epigenetic alteration occur under sterile conditions. However, humans sustain infection with viral, bacterial, fungal, and parasite pathogens across the course of a lifetime, many of which are capable of long-term persistence in host tissue and nerves. These pathogens—especially members of the human virome like herpesviruses, as well as intracellular bacteria and parasites—express proteins and metabolites capable of interfering with host immune signaling, mitochondrial function, gene expression, and the epigenetic environment. This paper reviews these and other key mechanisms by which infectious agents can accelerate features of human aging. This includes hijacking of host mitochondria to gain replication substrates, or the expression of proteins that distort the signaling of host longevity-regulating pathways. We further delineate mechanisms by which pathogen activity contributes to age-related disease development: for example, Alzheimer’s amyloid-β plaque can act as an antimicrobial peptide that forms in response to infection. Overall, because many pathogens dysregulate mTOR, AMPK, or related immunometabolic signaling, healthspan interventions such as low-dose rapamycin, metformin, glutathione, and NAD+ may exert part of their effect by controlling persistent infection. The lack of diagnostics capable of detecting tissue-resident pathogen activity remains a critical bottleneck. Emerging tools—such as ultrasensitive protein assays, cfRNA metagenomics, and immune repertoire profiling—may enable integration of pathogen detection into biological age tracking. Incorporating infection into aging models is essential to more accurately characterize drivers of senescence and to optimize therapeutic strategies that target both host and microbial contributors to aging.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102865"},"PeriodicalIF":12.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812769","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":"Group-based trajectory modelling for cognitive changes in middle-aged and older adults: A systematic review","authors":"Huan Zhang ,&nbsp;Hongli Chen ,&nbsp;Xiaotong Ding ,&nbsp;Qing Wang ,&nbsp;Jingjing Gu ,&nbsp;Shuaifang Wei ,&nbsp;Jiajun Xue ,&nbsp;Yulin Liang ,&nbsp;Zheng Li","doi":"10.1016/j.arr.2025.102855","DOIUrl":"10.1016/j.arr.2025.102855","url":null,"abstract":"<div><h3>Background</h3><div>Cognitive health constitutes a critical component of healthy aging. This study aims to review studies that employed group-based trajectory modeling approaches systematically to examine cognitive trajectories, identify associated determinants, and investigate the relationship with health outcomes.</div></div><div><h3>Methods</h3><div>A systematic search was performed in five databases for articles that identified two or more cognitive trajectories. The study was conducted following the PRISMA statement.</div></div><div><h3>Results</h3><div>Thirty-five studies, published from 2007 to 2024 across multiple countries, with sample sizes ranging from 318 to 19422 participants, were ultimately included in this study. The “High Stable” and “Moderate Decline” trajectories were the most frequently observed patterns. Key protective factors associated with the stable group included higher education, active lifestyle (e.g., cognitive/physical activities, high quality and appropriate duration of sleep, no smoking), and strong social networks. Older people with cardiovascular diseases, diabetes, and depression tend to experience rapid cognitive decline. Although relatively few studies have focused on biomarkers and brain structural changes, available evidence suggests that factors such as APOE ε4 carriage higher Aβ/global amyloid load, elevated t-tau+ , and entorhinal cortical thinning are associated with cognitive decline trajectories. In addition, several studies highlighted significant consequences linked to rapid cognitive deterioration, such as high incidence of dementia, mortality, and disability.</div></div><div><h3>Conclusion</h3><div>A substantial proportion of aging individuals maintain cognitive function over time, which may be supported by protective strategies like cognitive/physical engagement, healthy sleep, social connection, and disease management. The adverse outcomes linked to decline trajectories underscore the need for future research on modifiable factors. Comparing predictors across subgroups provides insights into cognitive resilience and proactive protection. Further exploration of biological measures is crucial for understanding cognitive aging and enabling earlier dementia prevention.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102855"},"PeriodicalIF":12.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812768","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":"Is the renin-angiotensin system a friend or foe in neurological diseases? Unveiling its role and therapeutic potential","authors":"Pratyush Porel ,&nbsp;Garry Hunjan ,&nbsp;Shamsher Singh ,&nbsp;Khadga Raj Aran","doi":"10.1016/j.arr.2025.102854","DOIUrl":"10.1016/j.arr.2025.102854","url":null,"abstract":"<div><div>The renin-angiotensin system (RAS), an important regulator of body fluid and cardiovascular homeostasis, is gradually implicated in the pathogenesis of neurological diseases due to its dysregulation. In addition to their traditional functions, components of the RAS, especially angiotensin-II (Ang-II), enhance neuroinflammation, oxidative stress, and neuronal injury. Ang-II exacerbates blood-brain barrier (BBB) disruption, promotes glial activation, and contributes to neurodegeneration via the Angiotensin type 1 (AT1) receptor (AT1R) and causes neurological diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), Huntington’s disease (HD), epilepsy, depression, and anxiety. The angiotensin (1−7) axis mediated by the Mas receptor appears to be neuroprotective, however, as it reverses the negative effects of Ang-II. In experimental models and clinical trials, blocking RAS specifically by angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) has demonstrated promise in reducing neuroinflammation and neuronal damage, especially in stroke and neurodegenerative diseases. In the current era of research, neuropharmacologists have new optimism due to emerging evidence of the promising potential of RAS-modulating drugs, such as ARBs and ACEIs, in the treatment of various neurological diseases. Since RAS imbalance causes neuroinflammation, neuronal damage, and cognitive decline in conditions including AD, PD, and MS, these drugs may offer a new treatment approach. In the current era of neuropharmacology, this technique is novel since it enables more targeted therapies to address the root causes of neurodegeneration. This review explores the molecular pathways of RAS dysregulation in various neurological diseases, highlighting its therapeutic potential and paving the way for future treatment strategies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102854"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779287","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":"Next-generation CRISPR gene editing tools in the precision treatment of Alzheimer’s and Parkinson’s disease","authors":"Harsh Kumar Meshram ,&nbsp;Sanjay Kumar Gupta ,&nbsp;Akash Gupta ,&nbsp;Kushagra Nagori ,&nbsp;Ajazuddin","doi":"10.1016/j.arr.2025.102851","DOIUrl":"10.1016/j.arr.2025.102851","url":null,"abstract":"<div><div>Emerging gene-editing technologies, such as the CRISPR system, represent a potential pathway for precision medicine targeting the genetic and molecular causes of diseases. Second-generation CRISPR technologies, including base editing, prime editing, and engineered Cas variants, have improved fidelity and offer alternative strategies for precise gene correction, transcriptional repression or activation, and modulation of pathological pathways in neurodegeneration. These tools can correct single-nucleotide mutations, reduce pathological protein accumulation, and modulate neuroinflammatory responses, all integral to the pathogenesis of Alzheimer’s disease (AD) and Parkinson’s disease (PD), both chronic, progressive neurodegenerative disorders. Unfortunately, currently available treatments are limited and primarily palliative. Preclinical studies have shown promising results, with improvements in cognitive and motor deficits in animal models. However, significant challenges must be addressed to ensure safe and effective delivery to the CNS, minimize off-target effects, and address ethical concerns. Current clinical investigations aim to translate these findings into available therapeutic options. This review also identifies the biological mechanisms, therapeutic use cases, and current limitations of next-generation CRISPR systems as tools in the context of AD and PD, providing both therapeutic and research capabilities through their unique strengths. Ultimately, the future of transactional neurogenomics will determine the clinical possibilities of CRISPR-based strategies for advancing neurodegenerative disease management beyond palliative and symptomatic treatment, toward a feasible mechanistic form of disease modification.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102851"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769366","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":"Meta-analyses of personality change from the preclinical to the clinical stages of dementia","authors":"Antonio Terracciano ,&nbsp;Martina Luchetti ,&nbsp;Selin Karakose ,&nbsp;Amanda A. Miller ,&nbsp;Yannick Stephan ,&nbsp;Angelina R. Sutin","doi":"10.1016/j.arr.2025.102852","DOIUrl":"10.1016/j.arr.2025.102852","url":null,"abstract":"<div><div>Personality changes are a clinical criterion for dementia diagnosis, yet their progression across disease stages remains unclear. This systematic review and meta-analyses examined change in the five major personality traits across the preclinical, transitional, and clinical dementia stages. We conducted pre-registered searches of three databases from their inception to November 2024. The standardized mean difference (SMD) with 95 % CIs were combined in random-effects meta-analyses. Prospective studies based on self-reports of personality (13 studies; N = 6895) found subtle changes in the preclinical and transitional stages (SMD = 0–0.2), which became more pronounced (SMD = 0.3–0.5) in the clinical stage. Retrospective studies based on informant ratings (26 studies; N = 1069) found smaller changes during mild cognitive impairment compared to dementia, with large (&gt;1 SMD) increases in neuroticism and decreases in extraversion and conscientiousness. Surprisingly, changes in frontotemporal dementia were slightly smaller than those observed in Alzheimer’s disease. By triangulating findings across study designs, we conclude that personality changes are subtle and inconsistent in the early preclinical stage. Personality changes become significant and pronounced as the disease progresses, in line with the rise of emotional and behavioral symptoms. Future multimethod studies should examine to what extent the rate of change is related to the underlying neurodegenerative processes. Our findings provide a framework for interpreting the timing and magnitude of non-cognitive changes in dementia, informing disease monitoring and targeted symptom management.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102852"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769365","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":"Beyond the 900-day rule: Reclaiming healthspan as geroscience’s primary goal","authors":"Stef F. Verlinden","doi":"10.1016/j.arr.2025.102857","DOIUrl":"10.1016/j.arr.2025.102857","url":null,"abstract":"<div><div>The recently proposed “900-day rule” in mouse aging studies—requiring lifespan extension over ultra-long-lived controls—aims to identify interventions that modulate intrinsic aging. While this standard raises scientific rigor, it may reduce relevance to how most organisms, including humans, actually age. In reality, aging unfolds under metabolically and immunologically stressful conditions—not in sterile, genetically uniform environments. Most people experience chronic inflammation, metabolic drift, and functional decline long before death. Prioritizing only pristine models risks overlooking the hallmarks of manifest aging: frailty, cognitive loss, immune erosion. This Viewpoint argues for a dual-track strategy: rigorous lifespan testing in ideal models should be complemented by phenotype-driven studies in real-world aging models—such as conventionally housed mice in academic settings—that reflect typical aging trajectories. Interventions like GlyNAC, NLRP3 inhibition, and CaAKG demonstrate broad functional benefits in real-world aging models—effects that may be dismissed as “noise” but are likely the most translationally meaningful. In the case of CaAKG, substantial reductions in frailty occurred even when lifespan gains were modest—highlighting the decoupling of healthspan from longevity. By embracing both intrinsic and manifest aging, geroscience can better target what matters most: improving healthspan for the many—not just lifespan for the few.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102857"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779286","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":"Age-dependent efficacy of Bifidobacterium strains on cognitive impairment and dementia: A systematic review and meta-analysis","authors":"Wenliang Yu ,&nbsp;Yao Li ,&nbsp;Zeyang Liu ,&nbsp;Siqi Hua ,&nbsp;Ziyi Tan ,&nbsp;Wei Tang ,&nbsp;Mengyue Gao ,&nbsp;Xiaoran Zhou ,&nbsp;Zichun Hua","doi":"10.1016/j.arr.2025.102850","DOIUrl":"10.1016/j.arr.2025.102850","url":null,"abstract":"<div><h3>Objective</h3><div>Cognitive impairment and dementia are prevalent and costly diseases, affecting 5–8 % of individuals aged 60 and above globally. <em>Bifidobacterium</em>, a low-cost probiotic, has shown potential in treating dementia, but its efficacy remains controversial. To investigate the effects of <em>Bifidobacterium</em> on various dementia-related functional tests and biomarkers in different patient populations with cognitive impairment and dementia.</div></div><div><h3>Methods</h3><div>Systematic searches were conducted on February 15, 2025, across Embase, PubMed, Medline, Wanfang, and ClinicalTrials.gov. The risk of bias was assessed using NOS. The study is registered with PROSPERO (CRD42023460809).</div></div><div><h3>Results</h3><div>After rigorous screening, 18 studies encompassing 1195 patients were included. The results revealed that <em>Bifidobacterium</em> significantly improved cognitive function (MMSE, WMD = 2.26, 95 % CI = 1.69–2.83, compared to placebo: p = 0.049), particularly in patients under 70 (MMSE, WMD = 2.81, 95 % CI = 1.97–3.65). For patients over 70, better outcomes were achieved without <em>B. breve</em>-based treatments (MMSE, WMD = 2.43, 95 % CI = 1.76–3.09, compared to the group age under 70 or the group over 70 and receiving <em>B. breve</em>-based treatments: p = 0.0133). Additionally, <em>Bifidobacterium</em> significantly enhance patients’ memory, language, visuospatial, attention and executive abilities, potentially through the downregulation of triglycerides (WMD = −19.52, 95 % CI = −32.28 to −6.66, p = 0.039) and MDA (SMD = −0.72, 95 % CI = −1.07 to −0.37, p = 0.0057).</div></div><div><h3>Conclusions</h3><div>These findings provide key insights into the efficacy of <em>Bifidobacterium</em>, supporting personalized treatment strategies and reducing the treatment burden for patients with cognitive impairment and dementia.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102850"},"PeriodicalIF":12.4,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144763946","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":"Exercise as elixir to combat cardiovascular ageing","authors":"Zihang Feng ,&nbsp;Yuan Xing ,&nbsp;Wei Yi ,&nbsp;Feng Gao ,&nbsp;Yang Sun ,&nbsp;Xing Zhang","doi":"10.1016/j.arr.2025.102848","DOIUrl":"10.1016/j.arr.2025.102848","url":null,"abstract":"<div><div>The global demographic shift towards an ageing population has rendered cardiovascular ageing and its associated pathologies a growing challenge for health. Emerging evidence highlights the critical role of exercise in mitigating age-associated cardiovascular alterations in structure and function and preventing ageing-associated cardiovascular diseases. However, the precise molecular mechanisms mediating these exercise-induced benefits in promoting healthy cardiovascular ageing remains incompletely mapped. Current progresses suggest that exercise exerts its anti-ageing effects through multiple synergistic mechanisms, including attenuation of conventional cardiovascular risk factors, cardiovascular structural remodeling, metabolic optimization, mitochondrial functional enhancement, and exerkine-mediated inter-tissue communication. These mechanisms collectively contribute to a more healthy cardiovascular ageing. Gaining a deeper insight into how exercise promotes healthy cardiovascular ageing not only advances our understanding of cardiovascular ageing but also illuminates potential approaches to prevent cardiovascular ageing and treat cardiovascular diseases. This review systematically discusses contemporary findings on exercise-mediated anti-cardiovascular ageing, and critically evaluates potential clinical applications and future research directions in the field.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102848"},"PeriodicalIF":12.4,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762639","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}