Aging Cell最新文献

{"title":"Sleeve Gastrectomy Improves Metabolic Health, Cognition, and Alzheimer's Disease Pathology in 3xTG Mice.","authors":"Reji Babygirija, Julia A Illiano, Michelle M Sonsalla, Grace Zhu, Christopher Retter Jabbarpour, Twinkle Mathew, Tristan Molkentin, Meredith Peterson, Carolyn Winder, Advaith Ravi Krishnan Nair, Fan Xiao, Justin M Wolter, Dudley W Lamming, David A Harris","doi":"10.1111/acel.70767","DOIUrl":"https://doi.org/10.1111/acel.70767","url":null,"abstract":"<p><p>Obesity and diabetes are well-established risk factors for Alzheimer's disease (AD), implicating metabolic dysfunction in AD pathogenesis. Sleeve gastrectomy (SG) is among the most effective metabolic interventions available, yet its impact on AD progression remains poorly understood. We hypothesized that SG performed early in life would improve metabolic health, attenuate AD pathology, and preserve cognition in a transgenic AD mouse model. Five-week-old female 3xTg-AD mice were preconditioned on a Western diet (WD) to induce obesity and glucose intolerance, then randomized to SG or sham surgery and maintained on either Control or continued WD for 12 months. Metabolic phenotyping, body composition, and cognitive assessments (Novel Object Recognition, Barnes Maze, Fear Conditioning) were performed longitudinally, with histological and molecular brain analysis at endpoint. Under Control-fed conditions, SG reduced fat mass and improved peripheral insulin sensitivity independent of food intake. These changes were accompanied by reduced cortical Aβ plaque burden and attenuated astrocytic (GFAP) and microglial (IBA1) activation, specifically in the cortex. Mechanistically, SG altered the insulin signaling-autophagy axis in a region-specific manner, with increased pAKT and suppressed ATG5/ATG7/ATG16L1 in the cortex. Under persistent WD, SG improved glucose homeostasis, reduced fat mass, lowered frailty, and rescued short- and long-term spatial memory deficits in the Barnes maze, accompanied by reduced cortical Aβ burden. Collectively, these findings provide the first preclinical evidence that SG attenuates AD progression through a brain insulin signaling-autophagy axis, supporting metabolic surgery as a promising disease-modifying intervention for AD prevention in individuals with obesity.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70767"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13660725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178102","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":"Skeletal Muscle-Derived Extracellular Vesicles in Interorgan Communication During Aging.","authors":"Weiyi Jiang, Kenon Chua, Joe Young, Eng King Tan, Hong-Wen Tang","doi":"10.1111/acel.70773","DOIUrl":"10.1111/acel.70773","url":null,"abstract":"<p><p>Skeletal muscle is increasingly recognized as a secretory organ that communicates with distant tissues through the release of bioactive factors, including extracellular vesicles (EVs). During aging, muscle-derived EVs have emerged as important mediators of interorgan communication, influencing tissue homeostasis, regeneration, metabolism, and disease progression. Recent studies demonstrate that skeletal muscle EVs carry diverse cargos such as proteins, lipids, metabolites, and regulatory RNAs that can modulate the function of recipient cells in multiple organs. In particular, aging-associated alterations in EV biogenesis, cargo composition, and secretion may contribute to chronic inflammation, stem cell dysfunction, metabolic decline, and age-related pathologies. In this review, we summarize current advances in skeletal muscle-derived EV biology and their roles in interorgan communication during aging. We discuss mechanisms regulating EV formation and cargo loading, their impact on stem cell function and tissue regeneration, and their involvement in aging-related diseases. We also highlight the translational potential of muscle EVs as biomarkers and therapeutic targets. Together, these findings identify muscle-derived EVs as key regulators of systemic aging and interorgan signaling.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70773"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178107","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":"Age-Associated Gut Microbiota Dysbiosis Impairs Antiviral Defense During Influenza Virus Infection and Identifies Acetate as a Protective Mediator in Senescent Human Lung Cells.","authors":"Christoph Wernike, Antje Häder, Yasmina Reisser, Kiana Garakani, Franziska Hornung, Claude Jourdan Le Saux, Stefanie Deinhardt-Emmer","doi":"10.1111/acel.70750","DOIUrl":"10.1111/acel.70750","url":null,"abstract":"<p><p>Aging is associated with profound alterations in gut microbiota composition and function, including reduced production of short-chain fatty acids (SCFAs), yet it remains unclear whether these age-related microbial changes directly contribute to impaired antiviral defense during influenza A virus (IAV) infection. To address this question, we first characterized age-associated alterations of the gut microbiome and SCFA-related metabolic potential in a murine model of IAV infection. We then used a complementary human senescent lung fibroblast model to determine whether acetate, a major microbiota-derived SCFA, directly modulates antiviral responses in aging-associated lung cells. In old mice, IAV infection was associated with marked microbiota dysbiosis, including reduced abundance of SCFA-producing commensals such as Akkermansia muciniphila and Faecalibaculum rodentium, accompanied by decreased expression of microbial pathways involved in carbohydrate fermentation and acetate production. These findings suggested impaired microbiota-derived metabolic support of antiviral immunity during aging. Based on these observations, mechanistic studies in senescent human lung fibroblasts demonstrated that acetate supplementation significantly reduced viral replication and inflammatory responses. These protective effects were associated with FFAR2/FFAR3 signaling and enhanced histone H3 acetylation, indicating metabolic and epigenetic modulation of the antiviral response. Together, our findings establish a translational link between aging-associated gut microbiota dysfunction and impaired antiviral defense by combining a murine model of aging and influenza infection with mechanistic validation in human senescent lung cells. They identify acetate as a potential mediator of the gut-lung axis and support microbiota-targeted interventions to reduce influenza severity in older individuals.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70750"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13643650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126232","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":"uPAR-Targeting T Cell Engager Exerts Senolytic Effects in Mice and Non-Human Primates With Serum Aminotransferase Activity as a Safety Monitor.","authors":"Jian Deng, Xiaozhu Zeng, Jing Guo, Lihong Li, Shirui Zou, Nan Liu, Shuai He, Lanzhen Yan, Qiong Wang, Yongjie Zhu, Ben Wang, Dong Yang, Longbao Lv, Xudong Zhao","doi":"10.1111/acel.70742","DOIUrl":"10.1111/acel.70742","url":null,"abstract":"<p><p>Senolytic CAR-T cells targeting uPAR induce dose-dependent toxicities. Although dosage adjustment mitigates these toxicities in laboratory mice, clinical translation remains challenging owing to the unpredictability of CAR-T cell proliferation across heterogeneous patient populations. In contrast, bispecific T-cell engagers (BiTEs) offer a safer alternative with superior dose-titratability. Here, we have developed a GFD-CD3 BiTE by employing the growth factor-like domain (GFD) of the natural ligand uPA as the targeting moiety to target uPAR-positive senescent cells. Dose-range finding studies revealed that high-dose GFD-CD3 predominantly induced hepatotoxicity through T cell-mediated attack on hepatic endothelial cells. Crucially, under transaminase-guided monitoring, low-dose GFD-CD3 effectively eliminated senescent cells and alleviated age-related pathologies in aged mice and non-human primates without adverse effects. These findings establish GFD-CD3 as a clinically translatable senolytic agent and provide the compelling preclinical evidence for BiTE as a senolytic strategy.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70742"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149072928","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":"Endothelial TLR4 at the Crossroads of Vascular Senescence and Targeted Senotherapeutics.","authors":"Hyo-Jin Kim, Jeong-Hyung Lee, Cheol Hwangbo","doi":"10.1111/acel.70757","DOIUrl":"10.1111/acel.70757","url":null,"abstract":"<p><p>Traditionally viewed as a classic sentinel of innate immunity, Toll-like receptor 4 (TLR4) has emerged as a crucial pathological driver within the vascular endothelium, with its identity dictated by cell-type specificity, microenvironmental context, and fluctuating expression levels. This review critically examines the dual functional nature of endothelial TLR4, delineating how it transitions into a primary driver of vascular aging and organ-specific vascular pathologies. The profound spatial, temporal, and cellular heterogeneities of TLR4 signaling expose the fundamental inadequacies of conventional systemic pan-TLR4 blockade, which has repeatedly failed in clinical trials due to severe immunosuppression and metabolic disruptions. To bypass these limitations, we propose a precision senotherapeutic framework utilizing advanced drug delivery systems-such as Vascular cell adhesion molecule-1 (VCAM-1) or E-selectin-targeted nanoparticles and genetically engineered plant-derived exosomes-to compartmentalize TLR4 inhibition within pathologically altered endothelial sub-populations. By shifting the clinical paradigm from indiscriminate receptor suppression to spatiotemporal fine-tuning, this conceptual framework provides a rational blueprint for next-generation anti-aging therapies aimed at restoring vascular homeostasis throughout the aging process.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70757"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101622","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":"A Hypertrophic Stimulus Drives Age-Dependent Transcript Isoform Switching With and Without Differential Gene Expression in Skeletal Muscle.","authors":"Pieter J Koopmans, Abbey L Stokes, Christopher E Nelson, Yuan Wen, Ahmed Ismaeel, Kevin A Murach","doi":"10.1111/acel.70761","DOIUrl":"10.1111/acel.70761","url":null,"abstract":"<p><p>Aged skeletal muscle has a reduced ability to adapt to hypertrophic stimuli concomitant with dysregulation across several molecular layers. Whether altered RNA splicing associates with impaired adaptive potential is not well studied. We hypothesized that aging disrupts the splicing response to involuntary muscle mechanical loading. Using deep short-read Illumina RNA-sequencing (SRS, 60 million read pairs) and third generation Oxford Nanopore long-read RNA-sequencing (LRS) combined with a murine model of acute muscle mechanical overload (MOV), we illustrate how aged muscle has a reduced or possibly delayed potential for isoform switching in response to stress. SRS identified hundreds of genes with isoform switching events in adult MOV relative to sham but only 37 in aged MOV. LRS identified 19 genes (including Cacnb1, Naca, Psap) with true isoform switching in adult MOV and none in aged MOV. A subset of genes showed significant isoform switching without corresponding changes in overall gene expression, suggesting post-transcriptional regulation in response to MOV. These data highlight the importance of analyzing the transcriptome at the isoform level to uncover transcript diversity and \"unseen genes\" that may have unique functions and mechanisms influencing hypertrophic adaptations.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70761"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178037","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 Human Ovary Exhibits Dynamic Molecular Remodeling in the Decades Post-Menopause.","authors":"Mark A Watson, Bikem Soygur, Christina D King, Pooja R Devrukhkar, Simon Melov, Elisheva D Shanes, Mary Ellen G Pavone, Francesca E Duncan, Birgit Schilling","doi":"10.1111/acel.70714","DOIUrl":"10.1111/acel.70714","url":null,"abstract":"<p><p>The human ovary is among the first organs to show age-related functional decline, resulting in menopause. Beyond this transition, the postmenopausal ovary is often regarded as quiescent and remains poorly characterized. We analyzed the proteomes of healthy, non-pathological ovaries using mass spectrometry (data-independent acquisition) from 28 postmenopausal women (50-75 years old), stratified into three age groups (50-59, 60-69, ≥ 70). We quantified 5812 protein groups and observed progressive age-associated shifts, with 117 proteins significantly altered in the ≥ 70 versus 50-59 age comparison. Multivariate analysis demonstrated clear separation between 50-59 and ≥ 70-year-old age cohorts, with protein signatures shifting from RNA/gene-regulatory functions in younger ovaries to metabolic, trafficking, and innate immune/complement pathways in older ovaries. Across differential abundance, multivariate modeling, and covariate-adjusted linear modeling, we identified a convergent set of age-associated proteins that were integrated into the 26-protein Buck Postmenopausal Ovary Molecular Signature (BuckPOMS), a consensus molecular signature capturing progressive extracellular matrix remodeling, inflammatory signaling, and loss of structural and keratin-associated proteins with age. Representative BuckPOMS proteins, including the secreted matrisome proteins WNT4 and Fibromodulin (FMOD), were validated by immunohistochemistry. Pathway enrichment further identified an increase in inflammatory and matrisome pathways, and increased abundance of damage-associated secretory factors decades following menopause. These data fundamentally shift the notion of the postmenopausal ovary as an inert organ and instead demonstrate active and continuous molecular remodeling that has potential relevance to tissue signaling and implications for women's health.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70714"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178087","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":"Time-Restricted Feeding Delays Cardiovascular Aging by Increasing Acetic Acid Through Remodeling Gut Microbiota.","authors":"Man Liu, Mandi Luo, Yangyang Huang, Tianyi Ji, Yuman Wang, Qian Wang, Jie Huang, Tao Jiang, Cuntai Zhang, Tao Mi, Mian Cheng","doi":"10.1111/acel.70728","DOIUrl":"10.1111/acel.70728","url":null,"abstract":"<p><p>Time-restricted feeding (TRF) restricts food intake to daily windows, yet its efficacy against vascular aging and underlying mechanisms remain unclear. Here, we demonstrate that TRF attenuates angiotension II -induced accelerated vascular aging by reshaping gut microbiota, stabilizing microbial diversity, and elevating the Firmicutes/Bacteroidetes ratio. TRF preserved intestinal barrier integrity, upregulated tight junction proteins (Occludin, ZO-1, MUC2), reduced serum lipopolysaccharide, and suppressed systemic inflammation. These benefits translated into alleviated hypertension, aortic stiffness (reflected by pulse wave velocity), and pathological cardiac remodeling. Fecal microbiota transplantation recapitulated these effects, whereas antibiotic-induced microbiota depletion abolished TRF protection; importantly, exogenous acetate supplementation fully restored the phenotypes, establishing acetic acid as the critical downstream mediator. Mechanistically, acetic acid bound to GPR43, inhibited HDAC3, increased H4K8ac acetylation, blocked NLRP3-mediated pyroptosis, and reduced senescence markers (p53, p21, p16) in human umbilical vein endothelial cells, aorta, and heart. 16S rRNA sequencing and short - chain fatty acids metabolomic profiling further identified Limosilactobacillus as the primary acetic acid-producing bacterium enriched by TRF. Together, we uncover a Limosilactobacillus-acetic acid-GPR43/HDAC3/H4K8ac/NLRP3 axis, offering mechanistic insights into TRF as a non-pharmacological strategy against age-related cardiovascular diseases.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70728"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126210","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":"Inhibiting Glutaminase Reverses Senescence-Associated Mitochondrial Dysfunction and Skeletal Muscle Decline.","authors":"Hamsa Vardini Senthil Kumar, Debanik Choudhury, Pedro Lei, Pihu Mehrotra, Shahryar Shahini, Sydney Swedick, John Toftegaard, Stelios T Andreadis","doi":"10.1111/acel.70703","DOIUrl":"10.1111/acel.70703","url":null,"abstract":"<p><p>Age-associated loss of skeletal muscle mass and function, also known as sarcopenia, is closely linked to mitochondrial dysfunction. In this study, we report that senescent skeletal muscle myoblasts exhibit elevated activity and expression of the enzyme glutaminase (GLS1), which is mediated by p38 MAPK signaling and leads to intracellular urea accumulation that impairs mitochondrial function. Pharmacological inhibition of GLS1 with CB-839 reduced urea levels, restored the expression of electron transport chain (ETC) complexes, and improved mitochondrial function. Consistent with our in vitro findings, CB-839 administration to progeroid mice similarly upregulated ETC complexes and enhanced mitochondrial respiratory capacity in skeletal muscle, leading to improved structural integrity and enhanced muscle strength. Together, these findings suggest that targeting glutamine metabolism via GLS1 inhibition may represent a promising therapeutic strategy to ameliorate age-related skeletal muscle decline by restoring mitochondrial health.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70703"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13644385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126216","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":"Deep Learning Predicts Hematopoietic Stem Cell Aging From 3D Chromatin Images.","authors":"Pablo Iáñez Picazo, Eva Mejía-Ramírez, Dario Di Bari, Elena Vitali, Maria Carolina Florian, Paula Petrone","doi":"10.1111/acel.70656","DOIUrl":"10.1111/acel.70656","url":null,"abstract":"<p><p>The functional decline of the hematopoietic system during aging affects organismal function and contributes to reduced healthspan. Quantifying hematopoietic aging holds great scientific and clinical relevance. Alterations in chromatin architecture are a well-established hallmark of aging that encode rich and informative signatures of the aging process, yet they remain largely unexplored as quantitative markers. Here, we present an interpretable deep learning approach based on convolutional neural networks, ChromAgeNet, that learns changes in the spatial features of chromatin architecture upon aging of hematopoietic stem cells (HSCs). We trained our algorithm on 3D microscope images of DAPI-stained HSC nuclei to discriminate between young and aged murine HSCs, achieving an AUROC of 0.77 ± 0.03. This approach outperforms classical machine learning models trained on handcrafted chromatin features from the same dataset. We then applied explainable artificial intelligence techniques, identifying chromatin entropy, peripheral heterochromatin, and chromatin condensates as predictive markers. As a proof of concept, we evaluated the potential of our model as a phenotypic screening tool for aged HSCs treated with epigenetic drugs to detect rejuvenation. Altogether, we demonstrate that changes in chromatin organization can be modeled via machine learning to predict age-associated chromatin states in the hematopoietic compartment. Our developed framework, ChromAgeNet, serves as an interpretable algorithm to unravel the intricate relationship between chromatin changes and stem cell aging, and advance high-throughput drug screening for rejuvenation therapies.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70656"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068871","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}