Aging Cell最新文献

{"title":"Gut Metabolism Links Precision Nutrition, Exercise, and Healthspan in Drosophila melanogaster.","authors":"Fangchao Wei, Shiyu Liu, Yudong Sun, Haipeng Huang, Juan Liu, Fengzhong Wang, Bei Fan","doi":"10.1111/acel.70628","DOIUrl":"10.1111/acel.70628","url":null,"abstract":"<p><p>Longevity-promoting interventions commonly entail functional trade-offs, raising the unresolved question of whether lifespan extension necessarily compromises physiological performance. Here, utilizing a chemically defined diet (CDD) in Drosophila melanogaster, we systematically evaluated a multimodal intervention combining methionine restriction (MR), taurine supplementation (Tau), and moderate exercise. This combinatorial approach additively extended lifespan, preserved reproductive capacity, and improved locomotor function. Targeted metabolomics with stable isotope tracing revealed increased mitochondrial TCA cycle flux and enhanced gut redox homeostasis, suggesting these as central metabolic features. Notably, Lactiplantibacillus plantarum was found to be associated with the observed benefits, and recolonization experiments suggested that it partially accounts for the benefits conferred by MR-Tau combined with exercise, supporting a causal but partial role. Together, these findings support a \"nutrition-behavior-microbiota\" framework that uncouples the traditional trade-off between lifespan and functional health, offering new perspectives for promoting healthy aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 7","pages":"e70628"},"PeriodicalIF":7.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging-Related Muscle Bmal1 Decline Contributes to Bone Loss in Mice via Enhancing IL-1α-Mediated Osteoclastogenesis.","authors":"Kai Huang, Jun Qian, Yike Wang, Feng Zhang, Youjia Xu, Qiaocheng Zhai","doi":"10.1111/acel.70582","DOIUrl":"10.1111/acel.70582","url":null,"abstract":"<p><p>Osteoporosis, a common metabolic bone disorder linked to aging, is often accompanied by muscle degeneration. Muscle Bmal1 disruption in mice has been shown to affect various tissues, including the kidney, lung, and bone, indicating that the muscle molecular clock may influence the physiological homeostasis of multiple organs through systemic circulation. Despite this, the role of the muscle clock in age-related osteoporosis remains unclear. In aged mice, we observed a disruption in the circadian interaction between muscle and bone. Furthermore, both Bmal1 expression within muscle fibers and total BMAL1 protein levels in muscle tissue were significantly reduced. Using skeletal muscle-specific Bmal1 knockout mice, we observed osteoporosis-related phenotypes, including decreased bone mass and disrupted trabecular microarchitecture, along with disrupted diurnal expression of inflammatory cytokines. Mechanistically, we revealed that muscle Bmal1 deficiency impairs the rhythmic expression of the Hmox1 and induces the upregulation of IL-1α in muscle cells. The elevated circulating IL-1α promotes osteoclast differentiation, ultimately reducing bone mass. Importantly, the osteoporosis-related phenotype resulting from muscle Bmal1 knockout or aging was alleviated by nighttime time-restricted feeding (TRF), which reestablished a feeding-driven diurnal variation in Hmox1 expression within the muscle and reduced serum IL-1α levels. This study provides new insights into the pathogenesis of osteoporosis in the aging population. Furthermore, it suggests that TRF may offer a promising therapeutic strategy for treating osteoporosis in the elderly.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70582"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148203370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"iLDA-SGCN: Identifying Associations Between Age-Related Diseases and Long Non-Coding RNAs Using Dual Graph Convolutional Networks.","authors":"Yu Guo, Shizheng Qiu, Zhishuai Zhang, Jirui Guo, Haozheng Liang, Huanyu You, Fengjuan Lu, Yanwei Xu, Yang Hu","doi":"10.1111/acel.70572","DOIUrl":"10.1111/acel.70572","url":null,"abstract":"<p><p>Aging reshapes global disease burdens, yet the regulatory roles of long non-coding RNAs (lncRNAs) in age-related disorders remain incompletely characterized. We developed iLDA-SGCN, a graph-based computational framework that integrates singular value decomposition (SVD) with dual graph convolutional networks (GCNs) to predict lncRNA-disease associations. SVD first derives compact low-dimensional representations from the lncRNA-disease association matrix. Two complementary GCN modules then learn topology-aware embeddings: a correlation-map GCN operating on the bipartite lncRNA-disease network, and a similarity-map GCN operating on fused homogeneous graphs of lncRNAs and diseases constructed from MeSH semantic similarity and Gaussian association-profile kernels. Finally, association scores are estimated with an inner-product decoder optimized with a class-imbalance-aware loss function. Across five-fold cross-validation on LncRNADisease and MNDR datasets, iLDA-SGCN outperformed five competitive methods (SDLDA, LDNFSGB, IPCARF, LDASR, and LDA-VGHB) in terms of AUC (area under the ROC curve) and AUPR (area under the precision-recall curve). The model achieved AUC/AUPR of 0.960/0.968 on MNDR and 0.896/0.901 on LncRNADisease, with only a marginal precision shortfall versus LDA-VGHB on LncRNADisease. Ablation studies showed both GCN modules improved over a fully connected backbone, with the similarity-map GCN contributing the largest gains; the full model performed best overall. In case studies across eight prototypical age-related diseases, iLDA-SGCN identified HOTAIR, MALAT1, PVT1, MEG3, H19, LSINCT5, UCA1, and other candidates, yielding 33 candidates potentially involved in age-related disease mechanisms that require further experimental validation. Collectively, iLDA-SGCN integrates semantic and topological information to prioritize candidate lncRNA-disease associations related to aging, providing testable hypotheses for downstream mechanistic studies.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70572"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13249584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Evolving Landscape of Clinical Aging Clocks: From Epigenetic to Multi-Omics Integration.","authors":"Liying Liu, Yuanyuan Lai, Chunhui Tian, Yufei Huang, Jianheng Hao, Yuemeng Zhao, Dan Chen, Tianyu Wu, Daqian Zhou, Xiaoyan Zheng, Han Yang, Zheng Yu, Nihong Li, Jie Yang","doi":"10.1111/acel.70579","DOIUrl":"10.1111/acel.70579","url":null,"abstract":"<p><p>Aging clocks are tools that quantify biological aging through the integration of multi-omics data, encompassing epigenetic, transcriptomic, proteomic, metabolic, and microbial information, together with functional biomarkers. These tools show significant potential for use in preventive medicine, early detection of chronic conditions, and monitoring the effectiveness of interventions designed to enhance population health. The advancement of artificial intelligence has facilitated the widespread adoption of ensemble learning and deep learning techniques in constructing aging clocks. Such methods are capable of efficiently synthesizing and analyzing high-dimensional, multi-modal biological data, thereby uncovering deeper insights and promoting a transition from epigenetic-based aging prediction to the development of multi-omics and multi-modal aging clocks. Aging clocks built on large-scale data and artificial intelligence have demonstrated notable progress in terms of accuracy, interpretability, and generalizability. Consequently, they provide a substantive foundation for understanding mechanisms of aging and contribute meaningful guidance for clinical practices aimed at delaying age-related diseases and fostering healthy aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70579"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13271870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148262402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poorer Physical Function Is Associated With Elevated Spatial Entropy in the Aging Brain Network Landscape.","authors":"Clayton C McIntyre, Shannon M O'Donnell, Robert G Lyday, Jonathan H Burdette, Steven R Cummings, Stephen B Kritchevsky, Paul J Laurienti","doi":"10.1111/acel.70596","DOIUrl":"10.1111/acel.70596","url":null,"abstract":"<p><p>Life is a constant struggle against disorder. As we age, our ability to maintain internal order declines. In the healthy human brain, order is observable in the form of functionally segregated brain network communities that exhibit spatial consistency. These communities associate with distinct cognitive and physical functions. When mapped into the brain, they form a functional \"landscape\". We assessed the spatial disorder of these landscapes in older adults with a wide range of mobility using a spatial form of Shannon entropy. We found that compared to younger adults, older adults had significantly higher entropy in the sensorimotor cortex, basal ganglia, hippocampus, thalamus, and occipital lobe. Higher entropy in many of these regions was associated with worse physical function and higher body mass index in older adults. Findings suggest that spatial entropy in brain network landscapes may be a marker of declining physical function. Modifiable factors, such as losing excess weight, may help to ameliorate aging-related brain entropy increases in regions such as the sensorimotor cortex, which may in turn help to preserve physical function in older adults.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70596"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13277748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148275382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methionine Restriction Extends Yeast Lifespan by Activating Non-Nitrogen-Starvation-Induced Autophagy Through Limiting Methylation of Protein Phosphatase 2A.","authors":"Kaylah Birmingham, Nina Arslanovic, Thea Grauer, Ignacio Gutierrez, Ujani Chakraborty, Simone Sidoli, Jessica Tyler","doi":"10.1111/acel.70550","DOIUrl":"10.1111/acel.70550","url":null,"abstract":"<p><p>Methionine restriction (MR) extends the lifespan and healthspan of numerous eukaryotic organisms, but the molecular mechanisms at play are unclear. Here we find that the ability of MR to extend the budding yeast chronological and replicative lifespans is the consequence of reduced methionine conversion to the methyl donor S-adenosylmethionine (SAM). Mechanistically, the key antiaging event downregulated by MR is the methylation of protein phosphatase 2A (PP2A). In chronological aging cells under MR, unmethylated PP2A no longer dephosphorylates Npr2, a component of the SEACIT complex, resulting in activation of non-nitrogen-starvation (NNS)-induced autophagy. Deletion of genes encoding components of SEACIT or ATG1 (encoding a central player in the initiation of autophagy) blocked the ability of MR to extend lifespan, showing the critical role of the NNS-induced autophagy pathway in lifespan extension by MR. We identify the relevant Npr2 site dephosphorylated by PP2A as serine 362 and show that Npr2 phosphomimetic mutants are sufficient to extend chronological and replicative lifespan. Finally, we discover that MR only during the early stages of chronological aging is sufficient to prolong autophagy and extend lifespan. In addition to elucidating the molecular mechanism of MR-mediated lifespan extension, this study highlights potential therapeutic targets to achieve lifespan and healthspan extension in humans without the challenging long-term dietary changes required to achieve MR.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70550"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147979628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Brain-Derived Estrogen Is Associated With Sex- and Age-Dependent Alterations in Memory, Affective Behavior, and Hippocampal Extracellular Matrix Gene Expression.","authors":"Natalie C Piehl, Ariel W Halle, Guadalupe Rodriguez, Andrea Locci, Stacy Kujawa, Caroline Haywood, John Coon, Ross P McNally, Zaina A Karim, Tianming You, Hongxin Dong, Serdar E Bulun, Hong Zhao","doi":"10.1111/acel.70551","DOIUrl":"10.1111/acel.70551","url":null,"abstract":"<p><p>Nearly two-thirds of Americans with Alzheimer's disease (AD) are women. Prior research suggested that women with AD have lower brain estrogen levels than those without AD. However, how estrogen deficiency modulates this sex-based difference in AD vulnerability is not well understood. Aromatase, the key enzyme for estrogen biosynthesis, is expressed in both neurons and astrocytes of the brain, including the hippocampus. This study aims to assess the mechanistic link between brain-selective aromatase deficiency and sex-specific AD vulnerability. To achieve this goal, we used brain-specific aromatase knockout (bArKO) and whole-body total aromatase knockout (tArKO) mice of both sexes at young (6- to 8-month-old) and old (> 19-month-old) ages. We found that aromatase deletion decreased brain estrogen levels in bArKO mice and circulating and brain estrogen levels in tArKO mice. Impairment in spatial working memory and social interaction behavior was observed only in old female bArKO and tArKO mice. Both young and old female, but not male, tArKO mice displayed depression-like behavior. Bulk RNA-seq analysis of hippocampal tissues from young and old bArKO mice of both sexes revealed enrichment of extracellular matrix-related pathways and upregulated mRNA and/or protein expression of extracellular matrix-associated genes (e.g., Col1a1, Ccn2, Dcn, and Ogn) in old female bArKO mice compared to littermate control mice. These findings point to a novel link between local brain estrogen deficiency and sex- and age-specific extracellular matrix changes in the hippocampus of old bArKO female mice accompanied by AD-related memory and behavioral impairments.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70551"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148012694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urate-Related Genetic Risk Modulates the Anti-Aging Effects of Exogenous Nucleotides: Multi-Omics Evidence From Older Adults.","authors":"Ruisheng Fu, Shuyue Wang, Yuxiao Wu, Xueying Qin, Tao Huang, Yong Li, Meihong Xu","doi":"10.1111/acel.70581","DOIUrl":"10.1111/acel.70581","url":null,"abstract":"<p><p>Nucleotides-essential substrates for DNA repair, energy metabolism, and redox regulation-are emerging as nutritional modulators of biological aging. Yet, individual responses to exogenous nucleotide (NTs) supplementation remain poorly understood. Given that urate metabolism governs systemic oxidative balance, this study investigated whether genetic variability in urate regulation modifies the anti-aging effects of NTs. In this secondary analysis of the TALENTs randomized controlled trial (121 adults aged 60-70 years; 19-week intervention; NCT05243108), participants were stratified by urate polygenic risk score (UA-PRS) to evaluate genotype-dependent responses in DNA methylation age (DNAmAge) and leukocyte telomere length (LTL). A significant UA-PRS × intervention interaction was observed for ΔDNAmAge (p = 0.0114) and ΔLTL (p = 0.0271). NTs supplementation reduced DNAmAge in the High-PRS group (β = -5.10, p = 0.00013) and preserved telomere length in the Low-PRS group (β = 0.31, p = 0.0043). Multi-omics analyzes revealed that NTs modulated glucose-transport and pentose phosphate pathways in High-PRS individuals, while enhancing immune regulation and reducing GDF15 and IL-1β levels in Low-PRS individuals. These findings suggest that genetic variation in urate metabolism determines whether NTs are preferentially utilized for redox and epigenetic maintenance or for immune and inflammatory regulation, supporting a precision-nutrition model for delaying biological aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70581"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13249583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of SMARCAD1 Mitigates Tauopathy.","authors":"Vaishnavi S Jadhav, Rebecca L Kow, Asia D Beale, Misa Baum, Pamela J McMillan, Caitlin S Latimer, Nicole F Liachko, Brian C Kraemer","doi":"10.1111/acel.70543","DOIUrl":"10.1111/acel.70543","url":null,"abstract":"<p><p>Tauopathies are neurodegenerative diseases characterized by the accumulation of misfolded tau protein and include Alzheimer's disease (AD) and related dementia disorders. Identifying new strategies to treat tauopathy remains an important gap in the field. Using forward and reverse genetic approaches in C. elegans, we identified smrd-1, the C. elegans homolog of SMARCAD1, as a potent modifier of tauopathy phenotypes in a transgenic model of tauopathy. Loss of smrd-1 function rescues tauopathy-associated neuronal dysfunction and neurodegeneration in C. elegans models of tauopathy. Loss or reduction of smrd-1/SMARCAD1 decreases phosphorylated and total tau protein levels by reducing tau mRNA transcripts in C. elegans and mammalian HEK-tau cells. Loss of smrd-1 rescues tau-driven abnormal H3K9me3 chromatin methylation. Immunohistochemistry in human postmortem AD brain tissue showed SMARCAD1 depletion in a subset of cases that also exhibit depletion of MSUT2. Loss of smrd-1/SMARCAD1 rescues tau-mediated neurodegeneration via a tau mRNA lowering mechanism accompanied by changes in chromatin conformation.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70543"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148040325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opposing Association of Lung Neutrophils and PD-L1⁺ Monocytes in Age-Related Severity of SARS-CoV-2 Infection.","authors":"Serban Morosan, Clémence Granier, Noëlline Guillou, Selma Bennacer, Eléonore Weber-Delacroix, Julianne Peronnet, François Lanthiez, Sandrine Barthelemy, Christelle Enond, Jean-Luc Diehl, Elena Paillaud, Carine El-Sissy, Anne-Geneviève Marcelin, Vincent Calvez, Stéphane Marot, Amélie Guihot, Christophe Parizot, Karim Dorgham, Guy Gorochov, Christophe Combadière, Alexandre Boissonnas","doi":"10.1111/acel.70588","DOIUrl":"10.1111/acel.70588","url":null,"abstract":"<p><p>Advanced age is a major determinant of adverse outcomes during acute infections, yet the immunological mechanisms by which aging alters immune regulation and shapes disease trajectories remain poorly understood. Using SARS-CoV-2 infection as a model of acute viral challenge, we investigated how aging alters myeloid responses in the lungs. Across infected mouse models and human cohorts, disease severity was associated with a pronounced shift in myeloid balance, characterized by an increased neutrophil-to-monocyte ratio. Neutrophils exhibited prolonged retention within the pulmonary microvasculature and formed large co-aggregates with monocytes. In parallel, severe disease was associated with a defect in classical monocyte activation in the lungs, notably through reduced PD-L1 upregulation. This defect was not observed in the circulation, indicating tissue-dependent dysregulation of inflammatory and regulatory markers. Aging further accentuated this imbalance. Both aged mice and elderly patients displayed a reduced proportion of PD-L1-expressing lung monocytes, despite enhanced pulmonary neutrophil recruitment. This age-associated alteration distinguished severe from non-severe disease and characterized a maladaptive myeloid response to acute viral challenge. Together, these findings identify impaired, compartment-specific myeloid immune regulation as a central feature of age-related vulnerability to severe infection. They highlight that tissue-dependent regulatory failure compounds inflammatory excess as a key determinant of disease outcome and suggest that restoring myeloid regulatory function may offer therapeutic benefit in older individuals during acute respiratory infections.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 6","pages":"e70588"},"PeriodicalIF":7.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13261690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148222172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}