Aging Cell最新文献

{"title":"Tissue-specific functions of MSCs are linked to homeostatic muscle maintenance and alter with aging","authors":"Tamaki Kurosawa,&nbsp;Madoka Ikemoto-Uezumi,&nbsp;Yuki Yoshimoto,&nbsp;Keitaro Minato,&nbsp;Noriyuki Kaji,&nbsp;Takashi Chaen,&nbsp;Eiji Hase,&nbsp;Takeo Minamikawa,&nbsp;Takeshi Yasui,&nbsp;Kazuhide Horiguchi,&nbsp;Satoshi Iino,&nbsp;Masatoshi Hori,&nbsp;Akiyoshi Uezumi","doi":"10.1111/acel.14299","DOIUrl":"10.1111/acel.14299","url":null,"abstract":"<p>Mesenchymal stromal cells (MSCs), also known as fibro-adipogenic progenitors, play a critical role in muscle maintenance and sarcopenia development. Although analogous MSCs are present in various tissues, recent single-cell RNA-seq studies have revealed the inter-tissue heterogeneity of MSCs. However, the functional significance of MSC heterogeneity and its role in aging remain unclear. Here, we investigated the properties of MSCs and their age-related changes in seven mouse tissues through histological, cell culture, and genetic examinations. The tissue of origin had a greater impact on the MSC transcriptome than aging. By first analyzing age-related changes, we found that <i>Kera</i> is exclusively expressed in muscle MSCs and significantly down-regulated by aging. <i>Kera</i> knockout mice recapitulated some sarcopenic phenotypes including reduced muscle mass and specific force, revealing the functional importance of <i>Kera</i> in the maintenance of muscle youth. These results suggest that MSCs have tissue-specific supportive functions and that deterioration in these functions may trigger tissue aging.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 11","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337681","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":"Causal associations and shared genetic etiology of neurodegenerative diseases with epigenetic aging and human longevity","authors":"Yu Guo,&nbsp;Guojuan Ma,&nbsp;Yukai Wang,&nbsp;Tingyan Lin,&nbsp;Yang Hu,&nbsp;Tianyi Zang","doi":"10.1111/acel.14271","DOIUrl":"10.1111/acel.14271","url":null,"abstract":"<p>The causative mechanisms underlying the genetic relationships of neurodegenerative diseases with epigenetic aging and human longevity remain obscure. We aimed to detect causal associations and shared genetic etiology of neurodegenerative diseases with epigenetic aging and human longevity. We obtained large-scale genome-wide association study summary statistics data for four measures of epigenetic age (GrimAge, PhenoAge, IEAA, and HannumAge) (<i>N</i> = 34,710), multivariate longevity (healthspan, lifespan, and exceptional longevity) (<i>N</i> = 1,349,462), and for multiple neurodegenerative diseases (<i>N</i> = 6618–482,730), including Lewy body dementia, Alzheimer's disease (AD), Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Main analyses were conducted using multiplicative random effects inverse-variance weighted Mendelian randomization (MR), and conditional/conjunctional false discovery rate (cond/conjFDR) approach. Shared genomic loci were functionally characterized to gain biological understanding. Evidence showed that AD patients had 0.309 year less in exceptional longevity (IVW beta = −0.309, 95% CI: −0.38 to −0.24, <i>p</i> = 1.51E-19). We also observed suggestively significant causal evidence between AD and GrimAge age acceleration (IVW beta = −0.10, 95% CI: −0.188 to −0.013, <i>p</i> = 0.02). Following the discovery of polygenic overlap, we identified rs78143120 as shared genomic locus between AD and GrimAge age acceleration, and rs12691088 between AD and exceptional longevity. Among these loci, rs78143120 was novel for AD. In conclusion, we observed that only AD had causal effects on epigenetic aging and human longevity, while other neurodegenerative diseases did not. The genetic overlap between them, with mixed effect directions, suggested complex shared genetic etiology and molecular mechanisms.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 11","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277479","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":"In vitro immuno-prevention of nitration/dysfunction of myogenic stem cell activator HGF, towards developing a strategy for age-related muscle atrophy","authors":"Sakiho Tanaka,&nbsp;Alaa Elgaabari,&nbsp;Miyumi Seki,&nbsp;So Kuwakado,&nbsp;Kahona Zushi,&nbsp;Junri Miyamoto,&nbsp;Shoko Sawano,&nbsp;Wataru Mizunoya,&nbsp;Kenshiro Ehara,&nbsp;Naruha Watanabe,&nbsp;Yohei Ogawa,&nbsp;Hikaru Imakyure,&nbsp;Reina Fujimaru,&nbsp;Rika Osaki,&nbsp;Kazuki Shitamitsu,&nbsp;Kaoru Mizoguchi,&nbsp;Tomoki Ushijima,&nbsp;Takahiro Maeno,&nbsp;Takashi Nakashima,&nbsp;Takahiro Suzuki,&nbsp;Mako Nakamura,&nbsp;Judy E. Anderson,&nbsp;Ryuichi Tatsumi","doi":"10.1111/acel.14337","DOIUrl":"10.1111/acel.14337","url":null,"abstract":"<p>In response to peroxynitrite (ONOO⁻) generation, myogenic stem satellite cell activator HGF (hepatocyte growth factor) undergoes nitration of tyrosine residues (Y198 and Y250) predominantly on fast IIa and IIx myofibers to lose its binding to the signaling receptor c-met, thereby disturbing muscle homeostasis during aging. Here we show that rat anti-HGF monoclonal antibody (mAb) 1H41C10, which was raised in-house against a synthetic peptide FTSNPEVR_nitroY₁₉₈EV, a site well-conserved in mammals, functions to confer resistance to nitration dysfunction on HGF. 1H41C10 was characterized by recognizing both nitrated and non-nitrated HGF with different affinities as revealed by Western blotting, indicating that the paratope of 1H41C10 may bind to the immediate vicinity of Y198. Subsequent experiments showed that 1H41C10-bound HGF resists peroxynitrite-induced nitration of Y198. A companion mAb-1H42F4 presented similar immuno-reactivity, but did not protect Y198 nitration, and thus served as the control. Importantly, 1H41C10-HGF also withstood Y250 nitration to retain c-met binding and satellite cell activation functions in culture. The Fab region of 1H41C10 exerts resistivity to Y250 nitration possibly due to its localization in the immediate vicinity to Y250, as supported by an additional set of experiments showing that the 1H41C10-Fab confers Y250-nitration resistance which the Fc segment does not. Findings highlight the in vitro preventive impact of 1H41C10 on HGF nitration-dysfunction that strongly impairs myogenic stem cell dynamics, potentially pioneering cogent strategies for counteracting or treating age-related muscle atrophy with fibrosis (including sarcopenia and frailty) and the therapeutic application of investigational HGF drugs.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 10","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14337","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250032","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":"Xiao Lu,&nbsp;Dachuan Li,&nbsp;Zhidi Lin,&nbsp;Tian Gao,&nbsp;Zhaoyang Gong,&nbsp;Yuxuan Zhang,&nbsp;Hongli Wang,&nbsp;Xinlei Xia,&nbsp;Feizhou Lu,&nbsp;Jian Song,&nbsp;Guangyu Xu,&nbsp;Jianyuan Jiang,&nbsp;Xiaosheng Ma,&nbsp;Fei Zou","doi":"10.1111/acel.14346","DOIUrl":"https://doi.org/10.1111/acel.14346","url":null,"abstract":"<p>Cover legend: The cover image is based on the Article <i>HIF-1α-induced expression of the m6A reader YTHDF1 inhibits the ferroptosis of nucleus pulposus cells by promoting SLC7A11 translation</i> by Xiao Lu et al., https://doi.org/10.1111/acel.14210<figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 9","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14346","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231033","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":"Kerriann K. Badal,&nbsp;Abhishek Sadhu,&nbsp;Bindu L. Raveendra,&nbsp;Carrie McCracken,&nbsp;Sebastian Lozano-Villada,&nbsp;Amol C. Shetty,&nbsp;Phillip Gillette,&nbsp;Yibo Zhao,&nbsp;Dustin Stommes,&nbsp;Lynne A. Fieber,&nbsp;Michael C. Schmale,&nbsp;Anup Mahurkar,&nbsp;Robert D. Hawkins,&nbsp;Sathyanarayanan V. Puthanveettil","doi":"10.1111/acel.14347","DOIUrl":"https://doi.org/10.1111/acel.14347","url":null,"abstract":"<p>Cover legend: The cover image is based on the Article <i>Single-neuron analysis of aging-associated changes in learning reveals impairments in transcriptional plasticity</i> by Kerriann K. Badal et al., https://doi.org/10.1111/acel.14228 Image Credit: Phillip Gillette and Lynne Fieber\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":"23 9","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231035","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":"Blockade of dopamine D3 receptors improves hippocampal synaptic function and rescues age-related cognitive phenotype","authors":"Maria Rosaria Tropea,&nbsp;Marcello Melone,&nbsp;Domenica Donatella Li Puma,&nbsp;Valeria Vacanti,&nbsp;Giuseppe Aceto,&nbsp;Bruno Bandiera,&nbsp;Roberta Carmela Trovato,&nbsp;Sebastiano Alfio Torrisi,&nbsp;Gian Marco Leggio,&nbsp;Agostino Palmeri,&nbsp;Marcello D'Ascenzo,&nbsp;Fiorenzo Conti,&nbsp;Claudio Grassi,&nbsp;Daniela Puzzo","doi":"10.1111/acel.14291","DOIUrl":"10.1111/acel.14291","url":null,"abstract":"<p>Dopamine D3 receptors (D3Rs) modulate neuronal activity in several brain regions including the hippocampus. Although previous studies reported that blocking D3Rs exerts pro-cognitive effects, their involvement in hippocampal synaptic function and memory in the healthy and aged brain has not been thoroughly investigated. We demonstrated that in adult wild type (WT) mice, D3R pharmacological blockade or genetic deletion as in D3 knock out (KO) mice, converted the weak form of long-term potentiation (LTP1) into the stronger long-lasting LTP (LTP2) via the cAMP/PKA pathway, and allowed the formation of long-term memory. D3R effects were mainly mediated by post-synaptic mechanisms as their blockade enhanced basal synaptic transmission (BST), AMPAR-mediated currents, mEPSC amplitude, and the expression of the post-synaptic proteins PSD-95, phospho(p)GluA1 and p-CREB. Consistently, electron microscopy revealed a prevalent expression of D3Rs in post-synaptic dendrites. Interestingly, with age, D3Rs decreased in axon terminals while maintaining their levels in post-synaptic dendrites. Indeed, in aged WT mice, blocking D3Rs reversed the impairment of LTP, BST, memory, post-synaptic protein expression, and PSD length. Notably, aged D3-KO mice did not exhibit synaptic and memory deficits. In conclusion, we demonstrated the fundamental role of D3Rs in hippocampal synaptic function and memory, and their potential as a therapeutic target to counteract the age-related hippocampal cognitive decline.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 11","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138709","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":"Rejuvenation of the reconstitution potential and reversal of myeloid bias of aged HSCs upon pH treatment","authors":"Sachin Kumar,&nbsp;Jeffrey D. Vassallo,&nbsp;Kalpana J. Nattamai,&nbsp;Aishlin Hassan,&nbsp;Angelika Vollmer,&nbsp;Rebekah Karns,&nbsp;Mehmet Sacma,&nbsp;Travis Nemkov,&nbsp;Angelo D'Alessandro,&nbsp;Hartmut Geiger","doi":"10.1111/acel.14324","DOIUrl":"10.1111/acel.14324","url":null,"abstract":"<p>Aged hematopoietic stem cells (HSCs) show reduced reconstitution potential, limiting their use in transplantation settings in the clinic. We demonstrate here that exposure of aged HSCs ex vivo to a pH of 6.9 instead of the commonly used pH of 7.4 results in enhanced HSCs potential that is consistent with rejuvenation, including attenuation of the myeloid bias of aged HSC and restoration of a youthful frequency of epigenetic polarity. Rejuvenation of aged HSCs by pH 6.9 is, at least in part, due to alterations in the polyamine/methionine pathway within pH 6.9 HSCs, and consequently, attenuation of the production of spermidine also attenuated aging of HSCs. Exposure of aged HSCs to pH 6.9, or pharmacological targeting of the polyamine pathway, might thus extend the use of HSCs from aged donors for therapeutic applications.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 10","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138711","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":"Marcus Dittrich,&nbsp;Laura Bernhardt,&nbsp;Christopher A. Penfold,&nbsp;Thorsten E. Boroviak,&nbsp;Charis Drummer,&nbsp;Rüdiger Behr,&nbsp;Tobias Müller,&nbsp;Thomas Haaf","doi":"10.1111/acel.14331","DOIUrl":"https://doi.org/10.1111/acel.14331","url":null,"abstract":"<p>Cover legend: The cover image is based on the Article <i>Age-related and species-specific methylation changes in the protein-coding marmoset sperm epigenome</i> by Marcus Dittrich et al., https://doi.org/10.1111/acel.14200.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 8","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14331","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100370","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":"Modeling aging and retinal degeneration with mitochondrial DNA mutation burden","authors":"John Sturgis,&nbsp;Rupesh Singh,&nbsp;Quinn R. Caron,&nbsp;Ivy S. Samuels,&nbsp;Thomas Micheal Shiju,&nbsp;Aditi Mukkara,&nbsp;Paul Freedman,&nbsp;Vera L. Bonilha","doi":"10.1111/acel.14282","DOIUrl":"10.1111/acel.14282","url":null,"abstract":"<p>Somatic mitochondrial DNA (mtDNA) mutation accumulation has been observed in individuals with retinal degenerative disorders. To study the effects of aging and mtDNA mutation accumulation in the retina, a polymerase gamma (POLG) exonuclease-deficient model, the Polg^D257A mutator mice (D257A), was used. POLG is an enzyme responsible for regulating mtDNA replication and repair. Retinas of young and older mice with this mutation were analyzed in vivo and ex vivo to provide new insights into the contribution of age-related mitochondrial (mt) dysfunction due to mtDNA damage. Optical coherence tomography (OCT) image analysis revealed a decrease in retinal and photoreceptor thickness starting at 6 months of age in mice with the D257A mutation compared to wild-type (WT) mice. Electroretinography (ERG) testing showed a significant decrease in all recorded responses at 6 months of age. Sections labeled with markers of different types of retinal cells, including cones, rods, and bipolar cells, exhibited decreased labeling starting at 6 months. However, electron microscopy analysis revealed differences in retinal pigment epithelium (RPE) mt morphology beginning at 3 months. Interestingly, there was no increase in oxidative stress and parkin-mediated mitophagy in the ages analyzed in the retina or RPE of D257A mice. Additionally, D257A RPE exhibited an accelerated rate of autofluorescence cytoplasmic granule formation and accumulation. Mt markers displayed different abundance in protein lysates obtained from retina and RPE samples. These findings suggest that the accumulation of mtDNA mutations leads to impaired mt function and accelerated aging, resulting in retinal degeneration.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 11","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142102448","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 NLRP3 inhibitor Dapansutrile improves the therapeutic action of lonafarnib on progeroid mice","authors":"Inés Muela-Zarzuela,&nbsp;Juan Miguel Suarez-Rivero,&nbsp;Daniel Boy-Ruiz,&nbsp;Juan López-Pérez,&nbsp;Marta Sotelo-Montoro,&nbsp;Maria del Mar Navarrete-Alonso,&nbsp;Isidro G. Collado,&nbsp;José Manuel Botubol-Ares,&nbsp;Alberto Sanz,&nbsp;Mario D. Cordero","doi":"10.1111/acel.14272","DOIUrl":"10.1111/acel.14272","url":null,"abstract":"<p>The role of the inflammasomes in aging and progeroid syndromes remain understudied. Recently, MCC950, a NLRP3 inhibitor, was used in Zmpste24^−/− mice to ameliorate the phenotypes. However, the safety of MCC950 was questioned due to liver toxicity observed in humans. Nevertheless, inhibition of the inflammasomes would be a beneficial therapy for progeria. Here, we show that OLT1177 (dapansutrile), other NLRP3 inhibitor, improved cellular and animal phenotypes using progeroid fibroblasts and a Lmna^G609G/G609G mouse model. In both cases dapansutrile reduced progerin accumulation, NLRP3-inflammasome activation and secretory phenotype of senescence, extended the lifespan of progeroid animals, preserved bodyweight, and reduced kyphosis, inflammation, and senescence. Interestingly, dapansutrile further improved the effect of lonafarnib, the only FDA-approved drug for the progeria. The combination of both drugs reduced the inflammation and senescence, extended survival and ameliorated various progeroid defects both in vitro and in vivo, compared with treatment using lonafarnib alone. These findings and the safety of dapansutrile demonstrated in several clinical trials proposes it as a possible co-adjuvant treatment with lonafarnid in HGPS.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 9","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14272","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142078557","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}