Aging and Disease最新文献

{"title":"SCAP Interacts with Trim27 to Promote Vascular Neointimal Hyperplasia by Regulating the Stability and Ubiquitination of IκBα.","authors":"Yingcheng Yao, Xing Wang, Chengcheng Xuan, Da Li, Wenqin Huang, Li Wei, Xiong Z Ruan, Danyang Li, Yaxi Chen","doi":"10.14336/AD.2025.0584","DOIUrl":"https://doi.org/10.14336/AD.2025.0584","url":null,"abstract":"<p><p>Pathological vascular remodeling and intimal hyperplasia after vascular injury are representative pathological processes in age-associated vascular diseases. Previous data from our laboratory have indicated that sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) contributes to physiological angiogenesis during embryonic development. However, the role of SCAP in neointima formation is not fully understood. Here, we aimed to explore the mechanisms of SCAP in the proliferation and migration of vascular smooth muscle cells (VSMCs) during neointima formation after injury. We utilized three types of transgenic (Tg) mice to demonstrate that SCAP participates in the regulation of injury-induced neointima formation in the vascular wall by promoting the proliferation and migration of VSMCs. This novel function of SCAP is associated with the activation of the NF-κB/MMP2/9 signaling pathway. Importantly, we reported for the first time that SCAP activates the NF-κB pathway by promoting Trim27-mediated ubiquitination of the IκBα protein and accelerating its degradation, consequently activating MMP2/9 transcription, which resulted in migration and proliferation of VSMCs. We thus propose that SCAP/IκBα/NF-κB axis is a novel signaling pathway involved in the regulation of neointimal hyperplasia, and targeting this axis may have implications for preventing neointimal hyperplasia-related diseases.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Unhealthy Lifestyles with Cataract Risk, and The Mediating Role of Metabolic Signature: Analysis of the UK Biobank Prospective Cohort.","authors":"Jiao Qi, Kaimeng Su, Keke Zhang, Wenwen He, Jiaqi Meng, Yu Du Md, Yi Lu, Xiangjia Zhu","doi":"10.14336/AD.2025.0522","DOIUrl":"https://doi.org/10.14336/AD.2025.0522","url":null,"abstract":"<p><p>Emerging evidence has shown an association between certain unhealthy lifestyle factors and cataract risk. However, the synergistic effect of unhealthy lifestyle factors on cataract risk and their underlying mechanisms remains unknown. This study analyzed data from 199,415 baseline cataract-free participants from the UK Biobank prospective cohort study. Multivariable Cox proportional hazards models estimated the associations of individual unhealthy lifestyle factors (smoking, alcohol consumption, physical inactivity, unhealthy diet, and high body mass index) and their synergistic effect with cataract risk. Elastic net regression was performed to identify a metabolic signature reflecting unhealthy lifestyles, and the mediation effect was evaluated. Our results showed that only smoking and physical inactivity significantly increased cataract risk. Compared to the favorable lifestyle group, the cataract risk increased by 6% in the intermediate lifestyle group (95% confidence interval [CI]: 1.02-1.09) and by 14% in the unfavorable lifestyle group (95% CI: 1.08-1.20). The Cox regression model also revealed that the metabolic signature of unhealthy lifestyles was associated with cataract risk (adjusted hazard ratio, 1.31; 95% CI: 1.18-1.45). Mediation analysis demonstrated that the metabolic signature mediated the association between unhealthy lifestyles and cataract risk, with a mediation proportion of 18.01% (95% CI: 8.57-34.70%). Metabolic pathway analysis revealed that two metabolic pathways (fatty acids and lipoprotein particle concentration and size) played a crucial mediating role. Our study underscores novel insights into the effect of unhealthy lifestyle factors on cataract risk and the mediating role of metabolic factors in this process.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hip Fragility Fractures: One Or Two Pathologies? A Systematic Review and Meta-Analysis of Demographic, Diagnostic and Therapeutic Aspects.","authors":"José Luis Dinamarca-Montecinos, Miguel Yáñez, Ana Aguilera, Jean-Gabriel Minonzio","doi":"10.14336/AD.2025.0414","DOIUrl":"https://doi.org/10.14336/AD.2025.0414","url":null,"abstract":"<p><p>There is evidence that hip fragility fractures (HFF) are at least two different types of disease: intra- and extracapsular fractures (ICF and ECF). However, they are still mainly considered as one entity. Differentiating them may provide clues to improve their prevention, treatments and prognosis, and to reduce clinical, organisational and economic impacts. This work addressed published evidence about differences between ICF and ECF in older people, comparing demographic, etiologic, and therapeutic aspects, producing a summary of the state of the art, and determining which variables are associated with significant differences. A systematic review based on PRISMA methodology was conducted, searching in Google Scholar, Springer and Scopus from 01.01.1980 to 01.03.2024. Publications with p-values obtained from quantitative tests (p &;lt 0.05 statistically significant) were included. For meta-analysis, Weighted Mean Method was used. 51 studies (19 countries, 5 continents, 129,075 subjects) were included. 78.4% of main objectives was searching for differences between both HFF. 60.8% provide evidence for demographic variables; 29.4% for diagnostic variables; 11,8% for therapeutic variables. ECF occurred at an older age (p &;lt 0.05) in 43 studies (84.3%). There were no differences in sex (96.1%). 14 routine orthogeriatric blood parameters were studied. Haemoglobin, vitamin-B12, albumin and parathormone presented differences in &;gt50% of the studies. Surgical management was significantly different in all studies. Significant demographic, diagnostic and therapeutic differences exist between ICF and ECF. There is a lack of studies combining variables, especially haematological exams.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive Frailty and Health Care Utilization and Costs Among Middle-Aged and Older Adults: Findings from Four Longitudinal Cohort Studies.","authors":"Yemin Yuan, Zhenyu Shi, Xiaolong Guan, Yiqi Xia, Yanshang Wang, Huaxin Si, Ping He","doi":"10.14336/AD.2025.0722","DOIUrl":"https://doi.org/10.14336/AD.2025.0722","url":null,"abstract":"<p><p>Health care systems need better strategies to identify older adults at risk for costly care to select target populations for interventions to reduce health care burden. Cognitive impairment and frailty are among the two most common geriatric syndromes. We examined the association between cognitive frailty and health care utilization and costs. Participants aged 50 and over were drawn from four prospective cohorts of aging, including the China Health and Retirement Longitudinal Study (CHARLS), the Korean Longitudinal Study of Aging (KLoSA), the Mexican Health and Aging Study (MHAS), and the Survey of Health, Ageing and Retirement in Europe (SHARE). We classified participants according to their cognitive impairment and frailty status into the following groups: none, only cognitive impairment, only frailty and cognitive frailty. We used negative binomial regression models and sample selection models to explore the association between cognitive frailty and health care utilization and costs. Compared to participants without cognitive impairment and frailty, participants in the only frailty or cognitive frailty groups had higher average annual outpatient visits and inpatient admissions. Only cognitive impairment was significantly negatively associated with the probability of outpatient visits or out-of-pocket (OOP) costs. Only frailty was significantly associated with a higher probability of outpatient visits or more OOP costs. The association between cognitive frailty and outpatient visits varied by cohort. In KLoSA, cognitive frailty was associated with a lower probability of outpatient visits, whereas the other three cohorts show the opposite. Cognitive frailty was associated with higher outpatient costs in CHARLS, KLoSA and MHAS. Only frailty and cognitive frailty were associated with a higher likelihood of inpatient admission in each cohort, and they were also linked to higher inpatient costs in both KLoSA and SHARE. But cognitive frailty was associated with lower inpatient costs in MHAS. This study highlights the significant positive association between cognitive frailty and health care utilization and OOP costs in most countries. By recognizing the multifaceted nature of cognitive impairment and frailty, healthcare providers and policymakers can work towards more effective interventions and support systems that address the needs of middle-aged and older adults, ultimately improving their quality of life and reducing health care costs.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.","authors":"Chen Chen, Pengfei Chen, Wenxi Yu, Lingli Zhao, Yu Yang, Hua Qu, Changgeng Fu, Dazhuo Shi, Ming Guo","doi":"10.14336/AD.2025.0564","DOIUrl":"https://doi.org/10.14336/AD.2025.0564","url":null,"abstract":"<p><p>The prevalence of atrial fibrillation (AF), one of the most common cardiac arrhythmias, has significantly increased, especially within the aging population. Atrial fibrosis, a hallmark of the structural changes seen in AF, is characterized by abnormal activation and proliferation of atrial fibroblasts accompanied by excessive deposition of extracellular matrix. The initiation and progression of fibrosis are regulated by multiple profibrotic cytokines, with transforming growth factor-beta (TGF-β) serving as the primary mediator. Elevated expression and activation of TGF-β are frequently observed in myocardial diseases, where it drives myofibroblast differentiation, migration, and collagen production via the Smad-dependent and Smad-independent pathways. These fibrotic alterations disrupt normal atrial electrical conduction, thereby facilitating the onset and progression of AF. This review summarizes the role of TGF-β-mediated fibrotic remodeling in AF pathogenesis and treatment. We explored the molecular mechanisms underlying TGF-β signaling in atrial fibrosis, evaluated its potential as a predictive biomarker for AF and recurrence after ablation, and discussed therapeutic strategies targeting this pathway. Increasing evidence from studies on natural and synthetic TGF-β inhibitors highlights the potential of modulating this signaling cascade to attenuate fibrosis and enhance clinical outcomes. Our review underscores the pivotal role of TGF-β signaling in AF development and supports its potential as a promising target for therapeutic intervention capable of improving the efficacy of antiarrhythmic treatments.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apolipoprotein CII: Cornerstone of Pathophysiological Interplay in Aortic Stenosis and type 2 Diabetes Mellitus.","authors":"Nerea Corbacho-Alonso, Tamara Sastre-Oliva, Inés Perales-Sánchez, German Hernández-Fernandez, Emilio Blanco-López, Luis F López-Almodovar, Jorge Solis, Luis R Padial, Teresa Tejerina, Ana E Lopez-Jimenez, Laura Mourino-Alvarez, Maria G Barderas","doi":"10.14336/AD.2025.0518","DOIUrl":"https://doi.org/10.14336/AD.2025.0518","url":null,"abstract":"<p><p>Different studies have demonstrated that the progression from mild to severe calcific aortic stenosis (CAS) is faster in patients with type 2 Diabetes Mellitus (T2DM). Hence, we set out to find markers to improve the clinical management of individuals with both pathologies. Calcified and non-calcified valve tissue from patients with CAS, or with CAS and T2DM, was studied using a multiomics (proteomics and transcriptomics) strategy, highlighting the apolipoprotein CII (apoC2) protein as a potential biomarker. To define its diagnostic potential, we used ELISA and turbidimetry to measure the apoC2 in plasma from an independent cohort of patients. Moreover, an in vitro model of aortic valve interstitial cells (VICs) was used to evaluate the therapeutic potential of apoC2. This multiomics study demonstrated the increase in apoC2 protein and APOC2 gene expression in the valves of patients without T2DM. These changes were also reflected in their plasma, highlighting its potential as a diagnostic marker. Finally, exposure to recombinant apoC2 augments calcification and lipid deposition in VICs, effects that were dampened by silencing its expression, emphasizing the potential of apoC2 as therapeutic target. While the existence of T2DM affects the profile of the aortic valve, we have identified apoC2 as a potential diagnostic and therapeutic marker, an important step towards better clinical management that will help slow the progression of CAS in diabetic patients.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Dysfunction in Aging and Age-related Disorders.","authors":"Aida Adlimoghaddam","doi":"10.14336/AD.2025.10731","DOIUrl":"10.14336/AD.2025.10731","url":null,"abstract":"<p><p>Mitochondrial dysfunction is increasingly recognized as a unifying mechanism underlying aging and a wide range of age-related diseases. This special issue brings together recent advances that elucidate how impaired mitochondrial function contributes to neurodegenerative, cardiovascular, and metabolic disorders. The featured articles highlight molecular pathways of mitochondrial decline, its systemic consequences, and potential interventions aimed at restoring mitochondrial health. Collectively, these studies reinforce the concept that targeting mitochondrial integrity holds significant promise for promoting healthy aging and preventing chronic disease.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":"16 5","pages":"2495-2497"},"PeriodicalIF":6.9,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid Beta Regulates Astrocytic Glucose Metabolism and Insulin Signaling in Experimental Models of Alzheimer's Disease.","authors":"Melisa Bentivegna, Carlos Pomilio, Melina Bellotto, Nicolás González Pérez, Soledad P Rossi, Amal Gregosa, Daiana Vota, Fátima Merech, María Marta Bonaventura, Jessica Presa, Ángeles Vinuesa, Victoria Lux-Lantos, Soledad Porte Alcón, Flavia Saravia, Juan Beauquis","doi":"10.14336/AD.2025.0484","DOIUrl":"https://doi.org/10.14336/AD.2025.0484","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, characterized by amyloid beta (Aβ) plaques, neuroinflammation and cognitive impairment. Metabolic disturbances, particularly brain insulin resistance, are increasingly recognized as central features of AD pathophysiology. Astrocytes, essential for brain energy metabolism, exhibit a loss of homeostatic functions in AD, possibly promoting neurodegeneration. Even though the main astrocytic glucose transporters are non-insulin dependent, insulin may regulate astroglial glucose metabolism. Our objective was to evaluate insulin signaling and astrocyte metabolism in the PDAPP-J20 transgenic mouse model of familial AD and in mouse primary astrocyte cultures exposed to Aβ. Adult PDAPP-J20 mice showed hyperinsulinemia, hippocampal insulin resistance and astrocytic proinflammatory activation. The reactive glial phenotype was accompanied by decreased insulin receptor levels in this chronic setting. Exposure of primary astrocytes to Aβ induced proinflammatory activation, oxidative stress and loss of glutamate transporter EAAT2, crucial for neuroprotection. Even though Aβ-exposed astrocytes showed increased insulin receptor levels in this acute setting, insulin-induced phosphorylation of the receptor was hampered. Amyloid-treated astrocytes also showed increased glucose uptake, lactate release and glycogen storage. Insulin treatment was associated with a recovery of mitochondrial membrane potential and increased amyloid uptake, highlighting a pro-homeostatic role for the hormone. Our results highlight the interplay between insulin signaling and astrocyte metabolism at different experimental and temporal settings of amyloid pathology. Understanding these mechanisms may help to design therapeutic strategies aimed at restoring metabolic balance and mitigating neurodegeneration.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration and Application of Malignant Cell Heterogeneity Analysis with Single-Cell Transcriptome Sequencing Technology.","authors":"Wen Zhang, Tianliang Liu, Ting Liu, Yu Zhang, Zhenguo Zhao, Xinxin Zhang, Xiaoyang Li, Jiasheng Zhong, Zhicheng Li, Shifu Chen, Libin Xu","doi":"10.14336/AD.2025.0836","DOIUrl":"https://doi.org/10.14336/AD.2025.0836","url":null,"abstract":"<p><p>Cancer remains a formidable global health burden owing to its persistently high incidence and mortality, highlighting the need to elucidate its underlying biological mechanisms. Such insights are crucial for refining diagnostic precision and therapeutic efficacy. Notably, human tumors represent highly heterogeneous ecosystems, comprising a dynamic interplay between malignant cells and non-malignant components, such as immune infiltrates and stromal elements. This cellular heterogeneity constitutes a major obstacle in tumor research. Recent technological advancements have enabled the development and application of novel tools for investigating tumor heterogeneity. In this context, single-cell sequencing technologies emerged as transformative tools for dissecting tumor architecture at a cellular resolution, offering unprecedented insights into the cellular diversity and molecular underpinnings of cancer. In particular, single-cell RNA sequencing (scRNA-seq) has been widely used to analyze the tumor microenvironment, particularly its immune components, thereby providing a valuable framework for understanding tumor-immune system interactions. However, the intrinsic heterogeneity of tumor cells has received comparatively less attention, with limited studies focusing on these malignant populations. Comprehensive profiling of tumor cells has become increasingly feasible as scRNA-seq technologies continue to evolve, offering higher throughput, increased cell capture efficiency, and more advanced analytical pipelines. Despite these advancements, current applications of scRNA-seq remain primarily focused on immune and stromal cell populations. Therefore, a paradigm shift is warranted, redirecting the investigative focus toward tumor cells and gaining deeper insights into tumorigenesis and therapeutic vulnerabilities.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Burn Injuries Accelerate Biological Aging and Increase the Epigenetically Inferred Risk of Mortality and Frailty.","authors":"Fadi Khalaf, Serena Yang, Dalia Barayan, Diana Julia Tedesco, Michael Chong, Guillaume Paré, Marc G Jeschke","doi":"10.14336/AD.2025.0407","DOIUrl":"https://doi.org/10.14336/AD.2025.0407","url":null,"abstract":"<p><p>Biological aging is closely associated with heightened disease risk, frailty, and mortality. Interestingly, physical traumas, such as burn injuries, exhibit physiological effects that resemble those of aging. However, the impact of burn injuries on biological aging remains underexplored, creating a gap in the literature that could inform better prognosis and outcomes. We conducted a prospective cohort study to investigate the effects of burn injuries on various epigenetic clocks, including HorvathAge, GrimAge, PhenoAge, and DunedinPoAm, using whole blood. The study included 59 burn patients and 25 healthy controls and was validated using a murine model of thermal injury. Our study demonstrates that burn injuries accelerate biological aging and the rate of aging, with these effects persisting for up to 28 days post-injury. The extent of biological aging was positively correlated with burn size, with severe burns resulting in an acceleration of 13-14 years in biological age as measured by GrimAge and PhenoAge-double the acceleration observed with chronic long-term smoking. This acceleration occurred irrespective of age or sex, though older patients were the most vulnerable to the aging effects of burn injuries. The role of burns as an accelerator of aging was further confirmed in mice, which exhibited the equivalent of 3-6 human years of accelerated aging (8 mouse months, or 7 human days) after the injury, reinforcing the chronic nature of the effect. Additionally, burn injuries increased epigenetically inferred risks of frailty and mortality in humans, highlighting their long-term and enduring consequences. Collectively, our findings identify burn injuries as the most significant and chronic accelerant of biological aging reported to date. To our knowledge, this study is one of the first to link burn injuries-or any form of physical trauma-to accelerated cellular and biological aging.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}