Biogerontology最新文献

{"title":"Precision nutrition in epigenetic aging: SHAP-optimized machine learning identifies omega-3 constituent-specific associations with aging biomarkers.","authors":"Zhaoqi Yan, Yifeng Xu, Ting Peng, Xiufan Du","doi":"10.1007/s10522-025-10294-z","DOIUrl":"https://doi.org/10.1007/s10522-025-10294-z","url":null,"abstract":"<p><p>This cross-sectional investigation seeks to examine the association between dietary omega-3 fatty acids (including α-linolenic acid [ALA], eicosapentaenoic acid [EPA], and docosahexaenoic acid [DHA]) and biomarkers of cellular aging, specifically DNA methylation age (Horvathage) and telomere length (Horvathtelo), in older adults. Our analysis leveraged nationally representative data from 2,136 participants aged ≥ 50 years in the 1999-2002 NHANES cycles. Multivariable linear regression models with survey weights were constructed to evaluate dose-response relationships, complemented by restricted cubic splines (RCS) for nonlinearity detection. Machine learning optimization included comparative evaluation of nine algorithms through five-fold cross-validation, with model interpretability enhanced via SHapley Additive exPlanations (SHAP) analysis. Higher omega-3 intake (Tertile 3 [T3] vs Tertile 1 [T1]) demonstrated inverse associations with HorvathAge (β = -1.07), particularly for ALA intake (T3 ≥ 1.512 g/d: β = -1.11). Contrastingly, moderate-to-high omega-3 intake (T2 ≥ 0.917 g/d: β = 0.04; T3: β = 0.04) and individual components (ALA_T3: β = 0.04; DHA_T3 ≥ 0.041 g/d: β = 0.05; EPA_T3 ≥ 0.011 g/d: β = 0.03) exhibited positive correlations with HorvathTelo. RCS modeling revealed distinct patterns: linear inverse correlation for HorvathAge versus nonlinear J-shaped association with Horvathtelo. Among ML models, Linear Support Vector Machines achieved superior predictive performance. SHAP feature importance analysis consistently ranked omega-3 composite measures highest, followed by constituent components (ALA > DHA > EPA). Our findings suggest a potential dual role of omega-3 in biological aging modulation: higher intake associates with decelerated epigenetic aging while maintaining telomere length homeostasis. These observations underscore the importance of considering both composite measures and individual components in nutritional gerontology research.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"148"},"PeriodicalIF":4.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial light at night accelerates aging processes in pre-pubertal female rats.","authors":"Garima Yadav, Akanksha Singh, Amit Kumar Trivedi, Syed Ibrahim Rizvi","doi":"10.1007/s10522-025-10291-2","DOIUrl":"https://doi.org/10.1007/s10522-025-10291-2","url":null,"abstract":"<p><p>Urbanization has introduced multiple factors that promote circadian clock dependent or independent disruption of physiology. Conditions such as late-night light (ALAN) exposure, shift working, cross-continental traveling may lead to circadian dysregulation leading to obesity, metabolic disorders and physiological alterations. As ALAN affects the circadian clock with concomitant effects on stress and free radical physiology, we hypothesised that night exposure to artificial light may affect the rate of aging. We have investigated this by exposing pre-pubertal female rats to 15 days of artificial light at night (ALAN). A direct effect of ALAN on physiology was evident by the significant increase in body weight of ALAN exposed group. Consequently, biomarkers of aging: nitric oxide (NO), lipid peroxidation in terms of Malondialdehyde (MDA), protein carbonyl levels (PCO) and plasma membrane redox system (PMRS) were found to be significantly elevated in blood plasma. Increase of these parameters are positive indicators that ALAN may induce accelerated aging even in young animals by affecting their redox biology. Also, tissue specific expression of genes (TNFα, LC3β, NSE and SIRT1) which are established molecular correlates of healthy aging, metabolic rate, autophagy and normal antioxidant physiology were compared between ALAN exposed and control animals. Tissue specific effect on expression of TNFα, LC3β, NSE and SIRT1 was found when exposed to ALAN. These results highlight the negative effects of altered circadian rhythm on young rats. Our findings may find relevance to humans too, especially the very young and adolescent population, who are exposed to ALAN due to present lifestyle.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"149"},"PeriodicalIF":4.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of endothelial cell senescence via the miR-217/FOXO3 axis.","authors":"Yi-Sheng Khor, Pooi-Fong Wong","doi":"10.1007/s10522-025-10290-3","DOIUrl":"10.1007/s10522-025-10290-3","url":null,"abstract":"<p><p>The accumulation of senescent endothelial cells within the endothelium leads to vascular dysfunction. Independent studies have linked miR-217, a senescence-associated microRNA and FOXO3, a longevity factor, to cellular senescence in different study models. However, their roles and direct interaction in endothelial replicative senescence (RS) remain to be investigated. This study sought to investigate the role of miR-217/FOXO3 axis in endothelial cell senescence. Young and RS HUVEC models were established to determine the differential mRNA and protein expressions of miR-217 and FOXO3 by RT-qPCR and immunoblotting. HUVECs were transfected with miR-217 mimic duplexes and hairpin inhibitors to evaluate the effects of elevated or reduced miR-217 expressions in endothelial health. FOXO3 was also stably knocked down using a lentiviral vector and rescue experiments were performed. RS HUVECs showed elevated senescence markers and miR-217 but decreased FOXO3 expressions. Dual-luciferase reporter assay confirmed FOXO3 as a direct miR-217 target. MiR-217 overexpression reduced FOXO3 but increased p16INK4a protein levels and impaired angiogenic potential in young HUVECs, suggesting that miR-217 promotes endothelial senescence and hampers angiogenesis by targeting FOXO3. Suppressing miR-217 increased FOXO3 expression in both RS and early-stage senescence (ES) HUVECs. However, ES but not RS HUVECs exhibited improved angiogenic potential. Meanwhile, FOXO3 knockdown increased miR-217 and p16INK4a expressions, indicating that FOXO3 loss drives endothelial senescence. However, transfection of FOXO3 knockdown cells with miR-217 inhibitor could only partially recover HUVECs angiogenic potential, suggesting that FOXO3 is critical for maintaining endothelial function. Collectively, these results showed that endothelial senescence and angiogenic potential are mediated through the crucial interaction of miR-217/FOXO3.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"147"},"PeriodicalIF":4.4,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12279897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging influences protein digestion, absorption and amino acid metabolism.","authors":"Lili Qiu, Qianqian Huang, Wenhao Li, Qian Zhang, Jun Zhou, Juan Chen, Yixuan Li, Ran Wang, Pengjie Wang, Siyuan Liu, Bing Fang, Xiaoyu Wang","doi":"10.1007/s10522-025-10289-w","DOIUrl":"https://doi.org/10.1007/s10522-025-10289-w","url":null,"abstract":"<p><p>Proteins are essential biomolecules that play indispensable roles in maintaining cellular homeostasis and regulating systemic metabolic processes. Protein deficiency is closely associated with age-related chronic diseases. Our purpose is to reveal the reason of protein deficiency in the elderly and potential treatments. A systematic literature search mainly on human studies addressing gastrointestinal aging and amino acid homeostasis was conducted. This review investigated the effects of aging on protein metabolism and summarized age-related physiological changes that collectively disrupt protein homeostasis. These changes include reduced secretion of gastric acid and digestive enzymes, which impair protein digestion in the stomach and small intestine. Weakened intestinal motility further delays the transit of digested proteins, reducing the efficiency of amino acid absorption. Additionally, decreased function of amino acid transporter proteins in the intestines and muscles limits the availability of amino acids for protein synthesis. Impaired liver and kidney function exacerbates these issues by affecting amino acid catabolism and clearance. Together, these alterations lead to an imbalance in amino acid homeostasis, contributing to protein deficiency, increasing the risk of sarcopenia in the elderly. Overall, we highlight changes in protein digestion, absorption, and amino acid metabolism in the elderly, and gives the possibility of improving amino acid utilization efficiency in the elderly, paving the way for new treatments for age-related protein deficiency in the future.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"146"},"PeriodicalIF":4.4,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of mindfulness-based interventions on inflammaging: a systematic review and meta-analysis.","authors":"Xiaohong Huang, Jing Lv, Dongxu Zhu, Haining Peng, Tengbo Yu","doi":"10.1007/s10522-025-10287-y","DOIUrl":"10.1007/s10522-025-10287-y","url":null,"abstract":"<p><p>Mindfulness cultivates awareness, presence, and non-judgmental acceptance, enhancing overall well-being. Inflammaging, linking age and aged-related diseases, manifests through heightened levels of IL-6, TNF-α, and CRP, impacting aging indicators like TA, TL, PWV, and FMD. To assess how mindfulness-based interventions (MBIs) affect inflammaging, a search was conducted in PubMed, Web of Science, Cochrane Central Register, and ProQuest Dissertation & Theses Global up to March 2024. Criteria included English articles and dissertations with participants over 18. Selected studies were randomized controlled trials (RCTs) and pre-post trials evaluating biomarkers related to inflammaging. Standardized mean differences were calculated using Morris's d_ppc for RCTs and Cohen's d for uncontrolled pre-post trials. Eighty-nine studies were included. In RCTs, MBIs reduced levels of TNF-α (d_ppc = -0.40), IL-6 (d_ppc = -0.70), CRP (d_ppc = -0.48), and PWV (d_ppc = -0.30) while increasing FMD (d_ppc = 0.24), TL (d_ppc = 0.43) and TA (d_ppc = 0.84). Pre-post trials indicated MBIs reduced TNF-α (d_ppc = -0.17), IL-6 (d = -0.33) and CRP (d = -0.33). Moderator analyses highlighted that MBIs other than mainstream mindfulness practices were found to be more effective in reducing IL-6 and CRP, and MBIs were particularly effective in reducing TNF-α among those with diseases. The main analysis revealed moderate certainty evidence from RCTs and uncontrolled pre-post trials supporting a causal relationship between mindfulness practices and inflammaging-related responses. The findings suggest that exploring alternative types of MBIs beyond mainstream approaches may yield more sustained benefits in attenuating inflammaging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"145"},"PeriodicalIF":4.4,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-dependent geroprotective effects of malvidin in Drosophila melanogaster.","authors":"Denis Golubev, Elena Platonova, Nadezhda Zemskaya, Oksana Shevchenko, Mikhail Shaposhnikov, Polina Tumaeva, Sergey Patov, Alexey Moskalev","doi":"10.1007/s10522-025-10285-0","DOIUrl":"https://doi.org/10.1007/s10522-025-10285-0","url":null,"abstract":"<p><p>Malvidin-3-galactoside (M3G), an anthocyanin derived from  blueberries (Vaccinium myrtillus L.), is recognized for its antioxidant and anti-inflammatory properties. In this study, Drosophila melanogaster was treated with M3G at concentrations of 1, 10, and 100 µM, while control groups received an identical diet without M3G supplementation. Treatment with M3G extended the lifespan of male flies by as much as 5% (p < 0.05). However, in females, certain concentrations of M3G resulted in reduced lifespan and diminished stress resistance, highlighting sex-specific responses. M3G enhanced male stress resistance, particularly against oxidative stress (induced by paraquat), heat shock (35 °C), and gamma radiation (300 Gy), increasing their median survival by 13% (p < 0.01), 10% (p < 0.05), and 12% (p < 0.05), respectively. Furthermore, M3G exhibited antioxidant effects by lowering levels of reactive oxygen species (ROS) and preventing lipid peroxidation in vitro, with no observed cytotoxicity. Gene expression analysis revealed marked changes in genes related to oxidative stress response (sod1, keap1, nrf2), lipid metabolism (bmm, Lip3), and hypoxia (hif1), with more pronounced effects in males. These findings suggest that M3G holds promise as a geroprotective and antioxidant agent with sex-specific impacts on lifespan and stress tolerance.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"144"},"PeriodicalIF":4.4,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in brain remodeling, stem cell therapies, and translational barriers in stroke and brain aging.","authors":"Bogdan Capitanescu, Dirk M Hermann, Roxana Surugiu, Raphael Guzman, Denissa Greta Olaru, Aurel Popa-Wagner","doi":"10.1007/s10522-025-10282-3","DOIUrl":"10.1007/s10522-025-10282-3","url":null,"abstract":"<p><p>As the brain ages, it undergoes a series of molecular and cellular changes that affect its structure and function, contributing to age-related disorders-particularly cerebrovascular diseases and diminished regenerative capacity following ischemic injury. Despite significant research efforts, effective therapies for brain rewiring and functional recovery after cerebral ischemia remain elusive. A deeper understanding of the cellular and molecular mechanisms involved in the post-acute phase of stroke may help identify novel therapeutic strategies for age-associated vascular pathologies. Recent advances have highlighted several promising areas, including epigenetic modifications of the vascular wall, blood-brain barrier remodeling, cell- and subcellular-based therapies, and innovative delivery methods. However, despite encouraging preclinical findings, clinical trials have produced mixed results regarding the safety and efficacy of cell-based interventions. These outcomes suggest that successful stroke therapies in aging populations may require a multistage, integrative approach.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"143"},"PeriodicalIF":4.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroimmunology in ageing and longevity: a special collection issue of Biogerontology.","authors":"Gurcharan Kaur, Tamas Fulop, Arpita Konar, Jaspreet Singh","doi":"10.1007/s10522-025-10284-1","DOIUrl":"https://doi.org/10.1007/s10522-025-10284-1","url":null,"abstract":"<p><p>Ageing is associated with neuroimmune shifts from a resting to a hyperactive and inflammatory state, termed 'Neuroinflammageing', attributed to microglial priming, hyperactive astrocytes, cytokine and chemokine release, blood brain barrier leakage, and infiltration of peripheral immune cells. This special issue of Biogerontology on 'Neuroimmunology in Ageing and Longevity' brings together 11 reviews and original research papers dealing with the complex cross-talk between CNS and peripheral immune cells and molecules in the context of ageing. The articles compiled under this issue further address how understanding neuroimmune pathways may help to identify targets to design interventional regimens for healthy brain ageing and longevity.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"141"},"PeriodicalIF":4.4,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial dysfunction and aging: multidimensional mechanisms and therapeutic strategies.","authors":"Pei Wei, Xiaoyan Zhang, Chi Yan, Siyu Sun, Zhigang Chen, Fei Lin","doi":"10.1007/s10522-025-10273-4","DOIUrl":"10.1007/s10522-025-10273-4","url":null,"abstract":"<p><p>Aging is an inherent phenomenon that is highly important in the pathological development of numerous diseases. Aging is a multidimensional phenomenon characterized by the progressive impairment of various cellular structures and organelle functions. The basis of human organ senescence is cellular senescence. Currently, with the increase in human life expectancy and the increasing proportion of the elderly population, the economic burden of diseases related to aging is becoming increasingly heavy worldwide, and an in-depth study of the mechanism of cellular aging is urgently needed. Aging, a multifactor-driven biological process, is closely related to mitochondrial dysfunction, which is the core pathological basis of a variety of age-related diseases. This article systematically reviews the molecular pathways by which mitochondrial dysfunction drives aging through multidimensional mechanisms such as metabolic reprogramming, epigenetic regulation, telomere damage, autophagy imbalance, and the senescence-associated secretory phenotype. Metabolic reprogramming promotes tumor progression and exacerbates energy metabolism disorders through abnormal activation of the PI3K/Akt/mTOR signaling pathways. The sirtuin family (such as SIRT1 and SIRT3) maintains mitochondrial homeostasis by regulating PGC-1α, FOXO3 and other targets. Telomere shortening directly inhibits mitochondrial biosynthesis through the p53-PGC-1α axis, leading to oxidative stress accumulation and a decline in organ function. The dual roles of autophagy (removing damaged mitochondria or inducing apoptosis) suggests that its homeostasis is essential for delaying aging. The SASP mediates the inflammatory microenvironment through the cGAS‒STING pathway, which is not only a marker of aging but also a driving force of disease progression. Future studies need to integrate multiomics techniques to analyze the interaction network between mitochondria and other organelles, such as the endoplasmic reticulum and lysosomes, and explore precise intervention strategies targeting sirtuins, AMPK and telomerase. Combined therapies targeting metabolic reprogramming or SASP inhibition are expected to provide new ideas for delaying aging and preventing age-related diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"142"},"PeriodicalIF":4.4,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bibliometric insights into the cell cycle, aging, and metabolism: from molecular mechanisms to clinical implications.","authors":"Yue Pan, Hao Liu, Jianni Chen, Hongsheng Deng, Chao Yang, Ying Huang, Qi Cai, Weitao Huang, Meiyu Huang, Shan Xiong, Huiting Liu, Linchong Huang, Haiqi Huang, Wenhua Liang, Jianxing He","doi":"10.1007/s10522-025-10271-6","DOIUrl":"10.1007/s10522-025-10271-6","url":null,"abstract":"<p><p>Cell cycle regulation, aging, and metabolism are pivotal biological processes linked to both normal physiology and disease development. Understanding their interplay is crucial for advancing gerontological research and clinical oncology. We analyzed articles and reviews on the cell cycle, aging, and metabolism from 2004 to 2023 using the Web of Science Core Collection. Bibliometric tools, VOSviewer, and CiteSpace, were applied to visualize collaboration networks, geographic distributions, and thematic clusters. Our analysis of 698 papers highlights a growing interest in the intersection of all three of these topics, with a notable publication surge from 2019 to 2022. The United States and China emerged as leading contributors, with significant international collaborations. Research themes evolved around molecular mechanisms, oxidative stress, and the implications for neurodegenerative diseases and cancer. Furthermore, keyword analysis identified five key clusters: neurodegenerative biomarkers, oxidative damage, cell cycle disruptions in cancer, epigenetic links between aging and cancer, and metabolic stress responses. Notably, metabolic shifts associated with aging influence both cellular repair mechanisms and the onset of senescence, indicating a transition from macroscopic changes to microscopic molecular alterations. This bibliometric study systematically maps the scholarly output on the cell cycle, aging, and metabolism, and our findings underscore the importance of molecular and genetic research in understanding the complex interactions and highlight their translational potential in oncology. Future research should explore personalized tumor treatment strategies based on individual cell cycle dynamics and genetic profiling.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"140"},"PeriodicalIF":4.4,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}