Biogerontology最新文献

{"title":"Neuroimmunology in ageing and longevity: a special collection issue of Biogerontology.","authors":"Gurcharan Kaur, Tamas Fulop, Arpita Konar, Jaspreet Singh","doi":"10.1007/s10522-025-10284-1","DOIUrl":"10.1007/s10522-025-10284-1","url":null,"abstract":"<p><p>Ageing is associated with neuroimmune shifts from a resting to a hyperactive and inflammatory state, termed 'Neuroinflammageing', attributed to microglial priming, hyperactive astrocytes, cytokine and chemokine release, blood brain barrier leakage, and infiltration of peripheral immune cells. This special issue of Biogerontology on 'Neuroimmunology in Ageing and Longevity' brings together 11 reviews and original research papers dealing with the complex cross-talk between CNS and peripheral immune cells and molecules in the context of ageing. The articles compiled under this issue further address how understanding neuroimmune pathways may help to identify targets to design interventional regimens for healthy brain ageing and longevity.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"141"},"PeriodicalIF":4.1,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial dysfunction and aging: multidimensional mechanisms and therapeutic strategies.","authors":"Pei Wei, Xiaoyan Zhang, Chi Yan, Siyu Sun, Zhigang Chen, Fei Lin","doi":"10.1007/s10522-025-10273-4","DOIUrl":"10.1007/s10522-025-10273-4","url":null,"abstract":"<p><p>Aging is an inherent phenomenon that is highly important in the pathological development of numerous diseases. Aging is a multidimensional phenomenon characterized by the progressive impairment of various cellular structures and organelle functions. The basis of human organ senescence is cellular senescence. Currently, with the increase in human life expectancy and the increasing proportion of the elderly population, the economic burden of diseases related to aging is becoming increasingly heavy worldwide, and an in-depth study of the mechanism of cellular aging is urgently needed. Aging, a multifactor-driven biological process, is closely related to mitochondrial dysfunction, which is the core pathological basis of a variety of age-related diseases. This article systematically reviews the molecular pathways by which mitochondrial dysfunction drives aging through multidimensional mechanisms such as metabolic reprogramming, epigenetic regulation, telomere damage, autophagy imbalance, and the senescence-associated secretory phenotype. Metabolic reprogramming promotes tumor progression and exacerbates energy metabolism disorders through abnormal activation of the PI3K/Akt/mTOR signaling pathways. The sirtuin family (such as SIRT1 and SIRT3) maintains mitochondrial homeostasis by regulating PGC-1α, FOXO3 and other targets. Telomere shortening directly inhibits mitochondrial biosynthesis through the p53-PGC-1α axis, leading to oxidative stress accumulation and a decline in organ function. The dual roles of autophagy (removing damaged mitochondria or inducing apoptosis) suggests that its homeostasis is essential for delaying aging. The SASP mediates the inflammatory microenvironment through the cGAS‒STING pathway, which is not only a marker of aging but also a driving force of disease progression. Future studies need to integrate multiomics techniques to analyze the interaction network between mitochondria and other organelles, such as the endoplasmic reticulum and lysosomes, and explore precise intervention strategies targeting sirtuins, AMPK and telomerase. Combined therapies targeting metabolic reprogramming or SASP inhibition are expected to provide new ideas for delaying aging and preventing age-related diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"142"},"PeriodicalIF":4.1,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12241157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bibliometric insights into the cell cycle, aging, and metabolism: from molecular mechanisms to clinical implications.","authors":"Yue Pan, Hao Liu, Jianni Chen, Hongsheng Deng, Chao Yang, Ying Huang, Qi Cai, Weitao Huang, Meiyu Huang, Shan Xiong, Huiting Liu, Linchong Huang, Haiqi Huang, Wenhua Liang, Jianxing He","doi":"10.1007/s10522-025-10271-6","DOIUrl":"10.1007/s10522-025-10271-6","url":null,"abstract":"<p><p>Cell cycle regulation, aging, and metabolism are pivotal biological processes linked to both normal physiology and disease development. Understanding their interplay is crucial for advancing gerontological research and clinical oncology. We analyzed articles and reviews on the cell cycle, aging, and metabolism from 2004 to 2023 using the Web of Science Core Collection. Bibliometric tools, VOSviewer, and CiteSpace, were applied to visualize collaboration networks, geographic distributions, and thematic clusters. Our analysis of 698 papers highlights a growing interest in the intersection of all three of these topics, with a notable publication surge from 2019 to 2022. The United States and China emerged as leading contributors, with significant international collaborations. Research themes evolved around molecular mechanisms, oxidative stress, and the implications for neurodegenerative diseases and cancer. Furthermore, keyword analysis identified five key clusters: neurodegenerative biomarkers, oxidative damage, cell cycle disruptions in cancer, epigenetic links between aging and cancer, and metabolic stress responses. Notably, metabolic shifts associated with aging influence both cellular repair mechanisms and the onset of senescence, indicating a transition from macroscopic changes to microscopic molecular alterations. This bibliometric study systematically maps the scholarly output on the cell cycle, aging, and metabolism, and our findings underscore the importance of molecular and genetic research in understanding the complex interactions and highlight their translational potential in oncology. Future research should explore personalized tumor treatment strategies based on individual cell cycle dynamics and genetic profiling.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"140"},"PeriodicalIF":4.1,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of MSCs and Muse cells: the possible use for healthspan optimization.","authors":"Mari Dezawa","doi":"10.1007/s10522-025-10275-2","DOIUrl":"10.1007/s10522-025-10275-2","url":null,"abstract":"<p><p>The exploration for safe, effective intervention strategies to improve longevity and aging-related diseases is attracting attention to prolong the healthy lifespan. Since aging is based on cellular changes, including telomere attrition, DNA damage, and mitochondrial dysfunction, therapies related to stem cells are expected to be a rational strategy for solving aging problems at the cellular level. Mesenchymal stem cells (MSCs) are an easily accessible, safe candidate, as they supply paracrine factors and extracellular vesicles to deliver pleiotropic effects for aging tissues. Multilineage-differentiating stress enduring (Muse) cells represent endogenous, reparative macrophage-like/pluripotent-like stem cells distributed in various tissues, including extraembryonic tissues such as the umbilical cord, and are also found in MSCs as a small percentage of the total population. Muse cell characteristics are different from those of MSCs. Intravenously injected Muse cells sharply sense the universal damage signal sphingosine-1-P and selectively migrate to damaged tissue rather than being trapped in the lung, phagocytose damaged/apoptotic cells in the tissue and directly differentiate into the same cell type. Muse cells then repair the three dimensional structure of the tissue by replacing multiple tissue component with healthy cells through pluripotent-like differentiation. Clinical trials have shown that HLA-mismatched donor Muse cells escape immune rejection and survive in the recipient tissue for an extended period without immunosuppressant treatment. Therefore, the pleiotropic bystander effects of Muse cells are more potent than those of MSCs. Due to heterogeneity, the properties of MSCs are still not fully understood; they have limited differentiation ability into osteogenic, chondrogenic, and adipogenic cells, and the main biological action in vivo is bystander effects. Muse cells are key, not only to the medical benefits of MSCs, but also to their potential use in anti-aging therapy. Enriching and purifying Muse cells will significantly enhance the therapeutic effect of MSCs, leading to further expansion of the use of MSCs. This review discusses the fundamental differences between MSCs and Muse cells and their potential applications in anti-aging therapy.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"139"},"PeriodicalIF":4.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The combination of hawthorn extract administration and high-intensity interval training (HIIT) alleviates hippocampus damage in aged rats: the behavioral, molecular and histological evaluations.","authors":"Mohammad Rami, Samaneh Rahdar, Hamid Aghili Nasab, Seyedeh Fatemeh Hoseininezhad, Seyedeh Narges Sadat Ahmadi, Mohammad Amin Rajizadeh","doi":"10.1007/s10522-025-10264-5","DOIUrl":"10.1007/s10522-025-10264-5","url":null,"abstract":"<p><p>The aging process results in a gradual decline in brain function, characterized by heightened hippocampal atrophy and dysfunction. Physical activity can enhance cognitive skills in elderly individuals and is significant in the prevention of neurodegenerative illnesses. Hawthorn (Crataegus oxyacantha) is a fruit-bearing shrub with a longstanding history as a medicinal agent. Currently, hawthorn is predominantly utilized for a range of pathological diseases. This research is designed to assess the neuroprotective impacts of exercise and hawthorn, both individually and together, on the hippocampus in the context of aging. Thirty male rats (24 old and six young) were allocated to six groups. In exercise groups, the animals underwent six weeks of treadmill exercise. Also, the treated rats with hawthorn extract received 100 mg/kg intraperitoneally. The open field and shuttle box tests were utilized to evaluate behavioral performance. Related kits measured the levels of MDA, SOD, and TNFα in the hippocampus. The western blotting method evaluated the protein expression of NFκB, COX2, and iNOS in the hippocampus. Also, the H&E, nissle, congo red, and tunnel stainings were utilized to investigate the hippocampus histology changes. Our results showed that following aging, the passive avoidance memory was impaired. Also, aging causes an increased level of oxidative stress and inflammation, as well as apoptosis and degeneration in the hippocampus tissue. However, HIIT and hawthorn extract could reduce inflammation and oxidative stress in the hippocampus. Also, the aging-induced histological changes were improved via HIIT and hawthorn extract administration.In conclusion, our findings revealed that six weeks of exercise and hawthorn extract can have neuroprotective effects following aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"137"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging expectations and science: a roadmap for the future of longevity interventions.","authors":"Danyang Yu, Xinyi Zeng, David Barzilai, Dominik Thor, Yu-Xuan Lyu","doi":"10.1007/s10522-025-10278-z","DOIUrl":"10.1007/s10522-025-10278-z","url":null,"abstract":"<p><p>The field of longevity interventions has witnessed rapid expansion, driven by scientific advancements alongside growing industry and consumer interest. However, no longevity intervention has yet been proven effective or ready for widespread clinical adoption. A substantial gap persists between public expectations and the current scientific realities. This article explores four key themes: (1) consumer priorities regarding longevity interventions, (2) the type and depth of scientific information they value, (3) psychological, financial, and practical barriers limiting adoption, and (4) potential strategies to overcome these challenges. Despite increasing enthusiasm, clinical translation of longevity research is constrained by the lack of validated interventions, regulatory frameworks, and standardized biomarkers. By distinguishing between scientifically supported and unproven approaches, this article proposes a roadmap outlining the critical milestones necessary to advance longevity interventions from research to clinical readiness. The goal is to realign public understanding with the current state of longevity science and guide future efforts toward safe and effective translation.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"138"},"PeriodicalIF":4.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12213962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synbiotic supplementation enhances memory processes in adult and aged male rats.","authors":"Débora Aguirre Gonçalves, Jordana Griebler Luft, Manuel Adrian Riveros Escalona, Michele Bertoni Mann, Jeverson Frazzon, Márcio Dorn, Pabulo Henrique Rampelotto, Lucas de Oliveira Alvares","doi":"10.1007/s10522-025-10267-2","DOIUrl":"10.1007/s10522-025-10267-2","url":null,"abstract":"<p><p>Synbiotic formulations, which combine prebiotics and probiotics in their composition, have shown promise in improving brain function and cognitive performance. However, the mechanisms by which synbiotics exert their beneficial effects on memory processes, particularly in the context of aging, remain unclear. In the present study, we investigated the effects of synbiotics supplementation on memory updating (reversal learning) and extinction in adult and aged rats. We also assessed the impact of the synbiotic intervention on the gut microbiota composition, diversity, and metabolism. The results showed that synbiotic supplementation (fructooligosaccharide and L. acidophilus, L. bulgaricius, L. casei, L. rhamnosus, and B. bifidum) improved memory updating in adult rats but not in aged rats. In contrast, the synbiotic facilitated memory extinction in aged rats, but not in adults. Interestingly, these cognitive benefits were not accompanied by significant alterations in the gut microbiome. This suggests that the synbiotic's effects on memory processes were mediated through more direct mechanisms, such as anti-inflammatory, antioxidant, and neuromodulatory actions, rather than through broad changes to the gut microbial community. These findings highlight the potential of synbiotic interventions to ameliorate age-related cognitive impairment and provide insights into the underlying mechanisms of the gut-brain axis.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"136"},"PeriodicalIF":4.1,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translational potential of GADD45α: biomarker and therapeutic target in age-associated neurodegeneration and longevity.","authors":"Imran Kazmi, Fahad A Al-Abbasi, Mustafa Zeyadi, Misbahuddin Rafeeq, Alaa Hamed Habib, Johar Iqbal, Sami I Alzarea, Omar Awad Alsaidan, Muhammad Shahid Nadeem","doi":"10.1007/s10522-025-10277-0","DOIUrl":"10.1007/s10522-025-10277-0","url":null,"abstract":"<p><p>Aging features a gradual decline in genomic integrity, epigenetic fidelity, and cellular homeostasis, driving the onset of chronic pathologies such as cancer, neurodegeneration, and metabolic disease. Growth arrest and DNA damage-inducible 45 alpha (GADD45α) functions as a pivotal stress-response mediator, coordinating DNA repair, cell-cycle arrest, oxidative stress defence, mitochondrial quality control, and chromatin remodeling. Researchers have extensively studied GADD45α in tumor suppression, but its roles in healthy aging and age-related disorders remain underexplored. Here, we provide a comprehensive synthesis of recent findings illuminating GADD45α's contributions to aging biology. We detail its engagement with nucleotide and base excision repair pathways to preserve genome stability, enforce G₂/M checkpoints to prevent damaged DNA propagation, and promote mitochondrial resilience under oxidative challenge. We then examine how GADD45α modulates epigenetic landscapes, mitigating age-associated DNA methylation drift and sustaining chromatin plasticity, and highlight its emerging neuroprotective actions in Alzheimer's and Parkinson's models. Integrating multi-omics analyses, in vivo rodent investigations, and Drosophila lifespan assays, we establish GADD45α as a dynamic biomarker of cellular aging and a promising geroprotective target. Finally, we discuss translational strategies to harness GADD45α activity, ranging from small-molecule enhancers and epigenetic modifiers to precision gene-editing to reinforce DNA repair capacity, delay senescence onset, and extend organismal healthspan. This review reframes GADD45α from a cancer-centric effector to a versatile regulator of aging processes, underscoring its therapeutic potential for promoting healthy longevity.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"135"},"PeriodicalIF":4.1,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pro-aging and rejuvenating effects of young and aged perivascular adipose tissues on endothelial function and inflammation.","authors":"Chak Kwong Cheng, Xingtao Huang, Shuhui Meng, Yu Huang","doi":"10.1007/s10522-025-10283-2","DOIUrl":"10.1007/s10522-025-10283-2","url":null,"abstract":"<p><p>Aging is considered as an independent risk factor for cardiovascular diseases. Common hallmarks of vascular aging include endothelial dysfunction, vascular inflammation, elevated oxidative stress, and telomere dysfunction. Perivascular adipose tissue (PVAT) is the local aggregate of adipose tissue surrounding the vascular bed, serving as a critical regulator of vascular function via either paracrine or endocrine manners. Aging-dependent malfunction of adipose tissues increases the risk of cardiometabolic diseases. Aging was previously shown to attenuate the anticontractile effect of PVAT in rodent arteries. Therefore, this study sought to understand whether aged and young PVAT promote and retard vascular aging in young and aged mice. PVAT-free aortas from aged and young mice were co-cultured with aortic PVAT from young and aged donor mice for 48 h, respectively. Endothelium-dependent relaxations (EDRs) in mouse aortas were determined by wire myography. Aged PVAT co-culture impaired endothelial function in the aortas of young mice, while young PVAT co-culture slightly alleviated endothelial dysfunction in aged mice. Aged PVAT co-culture induced vascular oxidative stress and inflammation, impaired telomere function, and suppressed AMPK/SIRT1 signaling in young mouse aortas. Conversely, these detrimental effects were partially reversed by young PVAT co-culture in aged mouse aortas. We further showed that these pro-aging and rejuvenating effects of PVAT were partially mediated by growth differentiation factor 15 (GDF15) and inflammatory cytokines. These findings highlight a substantial role of PVAT in modulating endothelial function and vascular aging, implying adipose-vascular axis as potential intervention target against cardiovascular aging and diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"134"},"PeriodicalIF":4.1,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of the Dicer family genes influences lifespan and stress resistance in a tissue-, sex-, and stressor-specific manner in Drosophila melanogaster.","authors":"Ekaterina Proshkina, Natalya Pakshina, Lyubov Koval, Evgeniya Shchegoleva, Nadezhda Zemskaya, Mikhail Shaposhnikov, Alexey Moskalev","doi":"10.1007/s10522-025-10272-5","DOIUrl":"10.1007/s10522-025-10272-5","url":null,"abstract":"<p><p>Small non-coding RNAs coordinate essential cellular processes, including gene expression regulation, genome stability maintenance, and transposon suppression. These processes determine aging, lifespan, and resistance of cells and organisms to stress. In this work, we conducted a comprehensive study of the geroprotective effects of overexpression of two Dicer family genes (Dcr-1 and Dcr-2, which are responsible for the biogenesis of miRNAs and siRNAs) in different tissues of Drosophila melanogaster (nervous system, fat body, intestine, muscles). Activation of the Dicer genes affected the lifespan in a tissue- and sex-depending manner. Females with Dcr-1 overexpression in the nervous system exhibited a significant and reproducible increase in both median (10.0-13.4%, p < 0.001) and maximum lifespan (10.0-13.4%, p < 0.01). However, in other cases, the effect was insignificant or negative. Additionally, flies with neuronal Dcr-1 activation had increased expression of several longevity genes (Sirt1, bsk, tgo, Gadd45, Xpc, Azot, foxo, Hsf, Tsc1) and significantly increased survival after acute exposure to 700 Gy γ-radiation (40-200%, p < 0.05). But they had reduced resistance to starvation. This indicates a crucial role of the miRNA machinery and the Dicer family in providing protection against genotoxic effects and coordinating metabolic processes.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"130"},"PeriodicalIF":4.1,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}