Aging Cell最新文献

{"title":"Smoking Promotes AT2 Cell Senescence and Exacerbates Pulmonary Fibrosis by Downregulating POT1 via Integratively Inducing CpG Methylation and MECP2-Mediated FOXP2 Transcriptional Binding Inhibition","authors":"Mengkun Shi,&nbsp;Wei Wang,&nbsp;Posum Wan,&nbsp;Jialun Shi,&nbsp;Huixia Cui,&nbsp;Zhonghan Sun,&nbsp;Xiaofeng Chen,&nbsp;Jingyu Chen,&nbsp;Jiucun Wang,&nbsp;Xiangguang Shi","doi":"10.1111/acel.70174","DOIUrl":"10.1111/acel.70174","url":null,"abstract":"<p>Smoking is one of the most recognized risk factors for pulmonary fibrosis (PF). However, the underlying mechanism is not well understood. This study reveals smoking increases the risk of developing idiopathic PF (IPF) and that smoked IPF patients exhibit higher levels of senescence markers than non-smoker IPF patients. Moreover, smoking enhances bleomycin (Bleo)-induced PF, along with obvious senescence of type II alveolar (AT2) cells. RNA-seq assay identifies cigarette downregulates protection of telomeres 1 (POT1), which is then validated to decrease in smoked PF patients and mice via upregulating the methyltransferase MECP2. Mechanistically, MECP2 binds to the DNA methyltransferases (DNMTs)-induced methylated CpG island in the POT1 promoter, and smoking inhibits the transcriptional activity of the CpG island. The transcription factor FOXP2 could bind to this CpG island to promote POT1 transcription. However, this process is inhibited by forming a MECP2−FOXP2 complex, which blunts the FOXP2−POT1 DNA binding. siRNA-mediated <i>POT1</i> knockdown promoted AT2 cell senescence in a p-ATM and p-ATR-dependent manner and secreted inflammatory and profibrotic factors, further promoting fibrotic response in fibroblasts. In vivo, delivery of the adeno-associated virus 9-POT1 (AAV9-POT1) vector inhibits cigarette-induced cell senescence and effectively alleviates PF in mice. These findings demonstrate that POT1 is an essential protector in PF by protecting against AT2 cell senescence.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 10","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70174","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673413","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":"Featured Cover","authors":"Estevão Scudese,&nbsp;Andrea G. Marshall,&nbsp;Zer Vue,&nbsp;Vernat Exil,&nbsp;Benjamin I. Rodriguez,&nbsp;Mert Demirci,&nbsp;Larry Vang,&nbsp;Edgar Garza López,&nbsp;Kit Neikirk,&nbsp;Bryanna Shao,&nbsp;Han Le,&nbsp;Dominique Stephens,&nbsp;Duane D. Hall,&nbsp;Rahmati Rostami,&nbsp;Taylor Rodman,&nbsp;Kinuthia Kabugi,&nbsp;Jian-qiang Shao,&nbsp;Margaret Mungai,&nbsp;Salma T. AshShareef,&nbsp;Innes Hicsasmaz,&nbsp;Sasha Manus,&nbsp;Celestine N. Wanjalla,&nbsp;Aaron Whiteside,&nbsp;Revathi Dasari,&nbsp;Clintoria R. Williams,&nbsp;Steven M. Damo,&nbsp;Jennifer A. Gaddy,&nbsp;Brian Glancy,&nbsp;Estélio Henrique Martin Dantas,&nbsp;André Kinder,&nbsp;Ashlesha Kadam,&nbsp;Dhanendra Tomar,&nbsp;Fabiana Scartoni,&nbsp;Matheus Baffi,&nbsp;Melanie R. McReynolds,&nbsp;Mark A. Phillips,&nbsp;Anthonya Cooper,&nbsp;Sandra A. Murray,&nbsp;Anita M. Quintana,&nbsp;Nelson Wandira,&nbsp;Okwute M. Ochayi,&nbsp;Magdalene Ameka,&nbsp;Annet Kirabo,&nbsp;Sepiso K. Masenga,&nbsp;Chanel Harris,&nbsp;Ashton Oliver,&nbsp;Pamela Martin,&nbsp;Amadou Gaye,&nbsp;Olga Korolkova,&nbsp;Vineeta Sharma,&nbsp;Bret C. Mobley,&nbsp;Prasanna Katti,&nbsp;Antentor Hinton","doi":"10.1111/acel.70170","DOIUrl":"https://doi.org/10.1111/acel.70170","url":null,"abstract":"<p>Cover legend: The cover image is based on the article <i>3D Mitochondrial Structure in Aging Human Skeletal Muscle: Insights Into MFN-2-Mediated Changes</i> by Estevão Scudese et al.,\u0000https://doi.org/10.1111/acel.70054\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 7","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70170","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647028","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":"Additional Cover","authors":"Sandra Atlante,&nbsp;Luca Cis,&nbsp;Davide Pirolli,&nbsp;Michela Gottardi Zamperla,&nbsp;Veronica Barbi,&nbsp;Antonello Mai,&nbsp;Clemens Zwergel,&nbsp;Serena Marcozzi,&nbsp;Maria Elisa Giuliani,&nbsp;Giorgia Bigossi,&nbsp;Giovanni Lai,&nbsp;Fiorenza Orlando,&nbsp;Robertina Giacconi,&nbsp;Fabrizia Lattanzio,&nbsp;Giulia Matacchione,&nbsp;Chiara Giordani,&nbsp;Massimo Bracci,&nbsp;Fabiola Olivieri,&nbsp;Federico Boschi,&nbsp;Paola Tabarelli De Fatis,&nbsp;Giovanni Battista Ivaldi,&nbsp;Marco Malavolta,&nbsp;Antonella Farsetti,&nbsp;Maria Cristina De Rosa,&nbsp;Carlo Gaetano","doi":"10.1111/acel.70171","DOIUrl":"https://doi.org/10.1111/acel.70171","url":null,"abstract":"<p>Cover legend: The cover image is based on the article <i>A Xanthine Derivative With Novel Heat Shock Protein 90-Alpha Inhibitory and Senolytic Properties</i>\u0000by Sandra Atlante et al., https://doi.org/10.1111/acel.70047.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 7","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70171","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647029","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":"Additional Cover","authors":"Tianpeng Zhang,&nbsp;Allancer D. C. Nunes,&nbsp;Jieun Lee,&nbsp;Dana Larocca,&nbsp;Giovanni Camussi,&nbsp;Sai Kiang Lim,&nbsp;Vicky U. Bascones,&nbsp;Luise Angelini,&nbsp;Ryan D. O'Kelly,&nbsp;Xiao Dong,&nbsp;Laura J. Niedernhofer,&nbsp;Paul D. Robbins","doi":"10.1111/acel.70173","DOIUrl":"https://doi.org/10.1111/acel.70173","url":null,"abstract":"<p>Cover legend: The cover image is based on the article <i>Identification of Senomorphic miRNAs in Embryonic Progenitor and Adult Stem Cell-Derived Extracellular Vesicles</i> by Tianpeng\u0000Zhang et al., https://doi.org/10.1111/acel.70071.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 7","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70173","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647031","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":"Anatomical Society Research Studentships 2025/26","authors":"","doi":"10.1111/acel.70178","DOIUrl":"https://doi.org/10.1111/acel.70178","url":null,"abstract":"","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 7","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144646942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Additional Cover","authors":"Muthu Saravanan Manoharan,&nbsp;Grace C. Lee,&nbsp;Nathan Harper,&nbsp;Justin A. Meunier,&nbsp;Marcos I. Restrepo,&nbsp;Fabio Jimenez,&nbsp;Sreenath Karekatt,&nbsp;Anne P. Branum,&nbsp;Alvaro A. Gaitan,&nbsp;Kian Andampour,&nbsp;Alisha M. Smith,&nbsp;Michael Mader,&nbsp;Michelle Noronha,&nbsp;Devjit Tripathy,&nbsp;Nu Zhang,&nbsp;Alvaro G. Moreira,&nbsp;Lavanya Pandranki,&nbsp;South Texas Veterans Health Care System (STVHCS) COVID-19 Clinical team,&nbsp;STVHCS COVID-19 Vaccine team,&nbsp;STVHCS COVID-19 Convalescent care team,&nbsp;STVHCS Center for Personalized Medicine,&nbsp;Sandra Sanchez-Reilly,&nbsp;Hanh D. Trinh,&nbsp;Clea Barnett,&nbsp;Luis Angel,&nbsp;Leopoldo N. Segal,&nbsp;Susannah Nicholson,&nbsp;Robert A. Clark,&nbsp;Weijing He,&nbsp;Jason F. Okulicz,&nbsp;Sunil K. Ahuja","doi":"10.1111/acel.70172","DOIUrl":"https://doi.org/10.1111/acel.70172","url":null,"abstract":"<p>Cover legend: The cover image is based on the article <i>The 15-Year Survival Advantage: Immune Resilience as a Salutogenic Force in Healthy Aging</i>\u0000by Muthu Saravanan Manoharan et al., https://doi.org/10.1111/acel.70063.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 7","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70172","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647030","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":"Beyond the Pseudogene: p17/PERMIT as a Mitochondrial Trafficking Protein Linking Aging and Neurodegeneration","authors":"Onder Albayram,&nbsp;Natalia Oleinik,&nbsp;Besim Ogretmen","doi":"10.1111/acel.70175","DOIUrl":"10.1111/acel.70175","url":null,"abstract":"<p>The misclassification of functional genomic loci as pseudogenes has long obscured critical regulators of cellular homeostasis, particularly in aging-related pathways. One such locus, originally annotated as RPL29P31, encodes a 17-kDa protein now redefined as PERMIT (Protein that Mediates ER–Mitochondria Trafficking). Through rigorous experimental validation—including antibody development, gene editing, lipidomics, and translational models—p17/PERMIT has emerged as a previously unrecognized mitochondrial trafficking chaperone. Under aging or injury-induced stress, p17 mediates the ER-to-mitochondria translocation of Ceramide Synthase 1 (CerS1), facilitating localized C18-ceramide synthesis and autophagosome recruitment to initiate mitophagy. Loss of p17 impairs mitochondrial quality control, accelerating neurodegeneration, and sensorimotor decline in both injury and aging models. This Perspective highlights p17 as a paradigm-shifting discovery at the intersection of lipid signaling, mitochondrial biology, and genome reannotation, and calls for a broader reassessment of the “noncoding” genome in aging research. We summarize a rigorous multi-platform validation pipeline—including gene editing, antibody generation, lipidomics, proteomics, and functional rescue assays—that reclassified p17 as a bona fide mitochondrial trafficking protein. Positioned at the intersection of lipid metabolism, organelle dynamics, and genome reannotation, p17 exemplifies a growing class of overlooked proteins emerging from loci historically labeled as pseudogenes, urging a systematic reevaluation of the “noncoding” genome in aging research.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 8","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70175","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648067","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-Dependent Histone Deacetylase 3 Regulation by βA3/A1-Crystallin and Inositol Hexaphosphate in Retinal Pigmented Epithelial Cells Reveals a Novel Pathway in Age-Related Macular Degeneration","authors":"Sujan Chatterjee,&nbsp;Sayan Ghosh,&nbsp;Zachary Sin,&nbsp;Vishnu Suresh Babu,&nbsp;Loretta Viera Preval,&nbsp;Emily Davis,&nbsp;Nguyen Tran,&nbsp;Sridhar Bammidi,&nbsp;Pooja Gautam,&nbsp;Stacey Hose,&nbsp;Yuri Sergeev,&nbsp;Miguel Flores-Bellver,&nbsp;Kevin Ritter,&nbsp;Henning J. Jessen,&nbsp;Issam Al Diri,&nbsp;Debasish Sinha,&nbsp;Prasun Guha","doi":"10.1111/acel.70163","DOIUrl":"10.1111/acel.70163","url":null,"abstract":"<p>Age-related macular degeneration (AMD), a leading cause of vision loss affecting retinal pigment epithelial (RPE) cells, remains largely unexplained by current genome-wide association studies (GWAS) risk variants. Our research on <i>Cryba1</i>, encoding βA3/A1-crystallin protein, reveals its crucial role in RPE cell function via a novel epigenetic mechanism, also evident in human atrophic AMD samples. Loss of <i>Cryba1</i> in mouse RPE cells triggers epigenetic changes by reducing histone deacetylase 3 (HDAC3) activity through two mechanisms. First, <i>Cryba1</i> depletion reduces inositol polyphosphate multikinase (IPMK) expression, which potentially reduces inositol hexakisphosphate (InsP6) generation since IPMK's kinase activity is essential for producing InsP4 and InsP5 as precursors to InsP6. Since InsP4, InsP5, or InsP6 is crucial for HDAC3's interaction with the corepressor's DAD domains, reduced IPMK expression in <i>Cryba1</i>-depleted cells likely diminishes the HDAC3-DAD interaction, leading to a reduction in HDAC3's activity. Second, reduced βA3/A1 protein in <i>Cryba1</i>-deficient cells impairs HDAC3's interaction with casein kinase 2 (CK2), resulting in decreased HDAC3 phosphorylation. Collectively, this increases H3K27 acetylation at the RET promoter region, likely enhancing the transcription of RET, a receptor tyrosine kinase critical for cell survival. Although RET is transcriptionally increased, <i>Cryba1</i> loss disrupts its protein maturation, causing immature RET protein accumulation. This triggers age-dependent endoplasmic reticulum (ER) stress, potentially contributing to the pathogenesis of AMD. Interestingly, although <i>Cryba1</i> is not identified as an AMD-linked variant in current GWAS, its loss may be linked to AMD mechanisms. These findings underscore the potential of gene-agnostic and epigenetic therapeutic strategies for treating AMD.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 9","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70163","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635785","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":"Even at 100+: Acute Exercise Modulates Inflammatory Pathways in Centenarians","authors":"Abel Plaza-Florido,&nbsp;Lidia B. Alejo,&nbsp;Inmaculada Pérez-Prieto,&nbsp;Pedro Carrera-Bastos,&nbsp;María Rosado Muñoz,&nbsp;Itziar Pagola Aldazabal,&nbsp;David Barranco-Gil,&nbsp;Alejandro Santos-Lozano,&nbsp;Gabriel Rodríguez-Romo,&nbsp;Natalia Yanguas-Casás,&nbsp;Shlomit Radom-Aizik,&nbsp;Alejandro Lucia,&nbsp;Carmen Fiuza-Luces","doi":"10.1111/acel.70152","DOIUrl":"10.1111/acel.70152","url":null,"abstract":"<p>Centenarians exhibit remarkable disease resilience despite chronic low-grade inflammation. We investigated the inflammation-related proteome response to acute exercise in seven centenarians (100–104 years). Exercise downregulated 52 proteins (e.g., TNF, IL10, IL1RN, CCL family members) involved in immune cell trafficking, apoptosis, and cytokine regulation. Even at the extreme end of the lifespan, humans retain molecular responsiveness to exercise, with modulation of inflammation-related pathways.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 9","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70152","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936849","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 Association Between Accelerated Biological Aging and the Physical, Psychological, and Cognitive Multimorbidity and Life Expectancy: Cohort Study","authors":"Zuliyaer Talifu,&nbsp;Ziyang Ren,&nbsp;Chen Chen,&nbsp;Shuai Guo,&nbsp;Yu Wu,&nbsp;Yuling Li,&nbsp;Binbin Su,&nbsp;Xiaoying Zheng","doi":"10.1111/acel.70142","DOIUrl":"10.1111/acel.70142","url":null,"abstract":"<p>As the global population ages, multimorbidity has become a critical public health issue. We analyzed 332,012 adults from the UK Biobank (2006–2022) to investigate the association between biological age—measured by the Klemera–Doubal method (KDM-BA) and phenotypic age (PhenoAge)—and a new comorbidity model encompassing physical, psychological, and cognitive disorders, with overall mortality outcomes over a median follow-up of 13.6 years. Logistic regression models examined the association between baseline health status and accelerated aging, while Cox proportional hazards models assessed mortality risk and disorder development. Cross-sectional analysis showed that accelerated aging was linked to higher comorbidity prevalence. Longitudinal follow-up revealed that individuals in the highest quartile (Q4) of aging speed (residual difference between estimated biological age and chronological age) had a 16%–17% higher risk of developing a single disorder, a 41%–44% higher risk of multimorbidity, and a 54% higher overall mortality risk compared with the lowest quartile (Q1). Among those with baseline single disorder, dual comorbidity, and triple morbidity, Q4 mortality risk increased by 89%–116%, 118%–166%, and 119%–156%, respectively. Multistate Markov models confirmed that accelerated aging (residual &gt; 0) increased the risk of transitioning to disorder, comorbidity, and death by 12%–37%. Individuals aged 45 with triple comorbidity lost an average of 5.3 years in life expectancy (LE), further reduced by 5.8 to 7.0 years due to accelerated aging. This study highlights that KDM-BA and PhenoAge robustly predict multimorbidity trajectories, mortality, and shortened LE, supporting their integration into risk stratification frameworks to optimize interventions for high-risk populations.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 9","pages":""},"PeriodicalIF":7.1,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144615580","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}