Bone Research最新文献

{"title":"Synovial inflammatory macrophage-derived extracellular vesicles exacerbate cartilage lesions with a FMRP-selectively sorted manner in osteoarthritis.","authors":"Shu Zhao, Jian Wang, Mengxin Xue, Baitong Wu, Lanyue Sheng, Yi Wen, Guangming Wang, Jianxing Song, Dajiang Du, Jun Xu","doi":"10.1038/s41413-025-00502-4","DOIUrl":"10.1038/s41413-025-00502-4","url":null,"abstract":"<p><p>Osteoarthritis (OA) is an aging-related degenerative joint disease without effective therapies. In the early stage of OA, mild synovitis has been reported to induce cartilage lesions. A better understanding of crosstalk between synovial macrophages and chondrocytes are being developed to discover new OA therapeutics. Here, we identified that the extracellular vesicles (EVs) derived from synovial pro-inflammatory macrophages regulated the autophagy function of chondrocytes, induced the onset of cartilage degeneration in normal joints. Mechanistically, the active transfer of miR-155-5p via EVs from synovial pro-inflammatory macrophages to chondrocytes accelerates cartilage degeneration by suppressing GSK-3β/mTORC1 axis-mediated autophagy function during OA progression. Deleting miR-155 from synovial pro-inflammatory macrophages relieved cartilage lesions and synovitis in OA mice. On the other hand, Fragile X mental retardation protein (FMRP) selectively sorted miR-155-5p into EVs derived from synovial pro-inflammatory macrophages, and the levels of plasma EVs FMRP were closely related to OA progression, suggesting the potential candidate for diagnostic OA biomarkers. Based on these findings, we developed engineering EVs with MAP (pro-inflammatory macrophages-affinity peptide) derived from adipose-derived stromal cells (ADSCs) as the antagomiR-155-5p delivery vehicles which exhibited superior therapeutic effects on synovitis and injured cartilage in the surgery-induced OA rats. Furthermore, MAP-ADSCs-EVs were proved to target the polarization of synovial pro-inflammatory macrophages in the clinical OA samples. Collectively, our study indicates that plasma EVs FMRP and engineered MAP-ADSCs-EVs targeting synovial pro-inflammatory macrophages represent potential novel therapeutic strategy for the progression of OA.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"26"},"PeriodicalIF":20.1,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12913794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146211659","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":"Smart biomaterials for skeletal aging repair and regeneration.","authors":"Dingfa Liang, Hufei Wang, Yu Jiang, Zeyuan Zhang, Tianjunke Zhou, Siliang Ge, Shuhuai Tan, Kaihua Qin, Yilin Wang, Xisheng Lin, Yong Xie, Houchen Lyu, Licheng Zhang","doi":"10.1038/s41413-026-00505-9","DOIUrl":"10.1038/s41413-026-00505-9","url":null,"abstract":"<p><p>Skeletal aging associated with diverse age-related disorders is increasing due to unhealthy diets, stressful lifestyles, and rapid aging. Repair and regeneration of aging skeletons are a global issue. Despite the self-healing ability of bone and the availability of various treatment strategies, degenerative bone repair and regeneration face significant problems due to unbalanced bone remodeling and a lack of active treatment strategies. The development of smart materials has created opportunities for degenerative bone repair and regeneration. The smart materials are responsive to endogenous/exogenous stimuli with tailored structure and function, which can promote skeletal aging repair and regeneration. Thus, in this study, skeletal aging is recognized as the progressive state that begins from peak bone mass to pathophysiological state and disorder conditions. We have introduced and characterized skeletal aging from the perspectives of cell-matrix-microenvironment and macrostructure-function-mechanical properties, for which systemic smart drug delivery systems and local smart scaffolds are designed. The smart drug delivery systems undergo conformation change and phase transition upon stimuli to release drugs at time- and site-specific to promote aging bone repair. Smart scaffolds with versatility and mechanical strength can replace bone defects to provide a tissue repair and regeneration microenvironment. Endogenous disease microenvironments and/or external physical triggers stimulate scaffold activation, which release bioactive factors to accelerate bone regeneration. This manuscript discusses the manufacturing techniques of these smart materials and presents key challenges and future directions for clinical translation, emphasizing their potential for personalized treatment and targeted therapy of skeletal aging.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"24"},"PeriodicalIF":20.1,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12905451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194038","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":"HIF-1α and BMAL1 in bone regeneration: crosstalk between hypoxia response and circadian rhythm.","authors":"Yihang Weng, Jiong Xiong, Qing Zhao, Zhen Tan","doi":"10.1038/s41413-026-00506-8","DOIUrl":"10.1038/s41413-026-00506-8","url":null,"abstract":"<p><p>Bone regeneration is initiated after a bone injury, such as a bone fracture or tooth extraction. It is a highly complex biological process involving multiple cell types, signaling molecules, and molecular pathways. The hypoxic microenvironment in the early stage of bone regeneration poses challenges to cell status and the final outcome of bone regeneration. During this phase, two key regulators-HIF-1α (the critical mediator of hypoxia response) and BMAL1 (the central component of the circadian rhythm)-orchestrate the activities of bone-regenerating cells, ensuring proper cellular function and orderly progression of bone repair. Existing studies have shown that there is a close crosstalk between HIF-1α and BMAL1, including regulation of gene expression, protein interaction, and regulation of downstream pathways. In this review, we discuss the respective regulatory roles of HIF-1α and BMAL1 in bone regeneration and further summarize their interactions within cells. Additionally, we extend the discussion to their interactions in other bone-related diseases, and summarize the existing research directions and deficiencies, providing new insights for in-depth studies of the hypoxia response and circadian rhythm systems.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"25"},"PeriodicalIF":20.1,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12906504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146197102","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":"Estradiol regulates osteoclast sialylation via ST3Gal1 in postmenopausal osteoporosis.","authors":"Ce Dou, Yang Dan, Ziyang Zhang, Xialin Li, Ying Qu, Yutong Wu, Zhongrong Zhang, Shuquan Guo, Jianzhong Xu, Fei Luo","doi":"10.1038/s41413-025-00498-x","DOIUrl":"10.1038/s41413-025-00498-x","url":null,"abstract":"<p><p>Estrogen deficiency after menopause accelerates bone loss by stimulating osteoclast formation and activity, but the molecular pathways that link estrogen signaling to osteoclast regulation remain incompletely defined. Here, we identify the sialyltransferase ST3GAL-I as a key mediator of RANKL-induced osteoclastogenesis. RANKL activates c-FOS to drive ST3GAL1 transcription, whereas estrogen-bound ERα competes with TRAF6 and suppresses this c-FOS-dependent induction. In a clinical cohort of pre-menopausal and post-menopausal women with or without osteoporosis, serum total and α-2,3-linked sialic acid levels increased with age and were highest in post-menopausal osteoporotic patients. Single-cell RNA sequencing of human bone revealed that osteoclasts form a prominent cluster only after menopause, where FOS, CTSK, and ST3GAL1 are strongly co-expressed, and the estrogen-responsive gene PGR is down-regulated. Additionally, in vivo experiments showed that sialidase treatment in estrogen-deficient models effectively reduced osteoclast-mediated bone loss, mimicking the effects of estradiol. These findings define a direct molecular link between loss of estrogen and activation of a FOS-ST3GAL1 sialylation pathway in osteoclasts, providing mechanistic insight into the enhanced bone resorption characteristic of post-menopausal osteoporosis.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"22"},"PeriodicalIF":20.1,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12901315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146177857","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":"Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.","authors":"Runze Zhou, Yixin Bian, Xuejie Cai, Hanyang Sun, Zehui Lv, Yiming Xu, Yingjie Wang, Han Wang, Wei Zhu, Bin Feng, Xisheng Weng","doi":"10.1038/s41413-025-00477-2","DOIUrl":"10.1038/s41413-025-00477-2","url":null,"abstract":"<p><p>Steroid-induced osteonecrosis of the femoral head (SONFH) is a debilitating condition resulting from the use of glucocorticoids, commonly prescribed for immune-related and inflammatory diseases. Understanding the mechanisms driving SONFH remains a significant challenge, complicating efforts to prevent and treat the condition. While genetic predispositions, impaired blood supply, and metabolic changes are recognized contributors, the complex interplay between these factors is not yet fully understood. Recent research has shed light on the pathogenesis of SONFH, exploring it from multiple perspectives, including tissue-level damage, cellular dysfunction, and molecular pathways. This review summarizes these recent advancements, providing an integrated understanding of the onset and progression of the condition. Additionally, it highlights emerging therapeutic strategies that potentially pave the way for more effective treatments in the future.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"23"},"PeriodicalIF":20.1,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12902040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146177842","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":"Pharmacological HIF activation protects against diet-induced obesity, glucose intolerance, and skeletal dysfunction by exerting dual beneficial effects on energy metabolism and bone","authors":"Roger Valle-Tenney, Nicolas Peredo, Karen De Samblancx, Elena Nefyodova, Ruben Cardoen, Tom Dehaemers, Delphine Farlay, Roland Chapurlat, Bart Van der Schueren, Chantal Mathieu, Roman Vangoitsenhoven, Christa Maes","doi":"10.1038/s41413-025-00503-3","DOIUrl":"https://doi.org/10.1038/s41413-025-00503-3","url":null,"abstract":"Obesity and type-2 diabetes, two interconnected and increasingly prevalent metabolic disorders, are associated with poor bone quality, higher fracture risk, and impaired fracture repair. The causes are not yet resolved but appear to relate to the impaired glucose homeostasis, altered bone material properties and remodeling, and compromised skeletal vascularization. Each of these features is impacted by hypoxia-inducible factor (HIF) signaling, which led us to hypothesize that HIF pathway modulation might be an effective strategy to concomitantly improve energy metabolism and bone health in conditions of metabolic stress. Here, we evaluated whether pharmacological HIF activation using the HIF-prolyl-hydroxylase-domain enzyme (PHD) inhibitor FG-4592 (Roxadustat) could protect mice against the adverse skeletal and metabolic consequences of high-fat diet (HFD)-induced obesity. We found that systemic FG-4592 treatment effectively prevented HFD-triggered body weight gain, glucose intolerance, and peripheral fat accumulation, associated with globally increased energy expenditure. Concomitantly, FG-4592 administration prevented the skeletal vascular damage, marrow fat accumulation, and bone formation deficits that were caused by HFD. Moreover, the HIF-activating drug also improved glucose metabolism and bone regeneration in a model of compromised fracture repair associated with overnutrition. Specifically, short-term FG-4592 treatment during fracture recovery reduced the body weight and fat mass of obese mice, improved glucose tolerance, and enhanced the fracture bridging capacity, along with promoting callus vascularization. These findings demonstrate that systemic hypoxia signaling stimulation using PHD inhibitors alleviates both the metabolic and skeletal consequences of diet-induced obesity in mice, highlighting its potential as a dual-action therapeutic strategy for enhancing glucose homeostasis and bone health/regeneration in disorders of obesity and metabolic dysfunction.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"95 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146152277","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":"Modeling the chondrocyte-derived osteoblasts formation process reveals its molecular signature and regulation network.","authors":"Raquel Ruiz-Hernández, Laurie Gay, Verónica Moncho-Amor, Pablo Martín, Jhonatan A Vergara-Arce, Stefania Di Blasio, Thomas Snoeks, Unai Cossío, Ander Matheu, Maria M Caffarel, Daniela Gerovska, Marcos J Araúzo-Bravo, Amaia Vilas, Felipe Prosper, Sergio Moya, Daniel Alonso-Alconada, Ana Alonso-Varona, Gretel Nusspaumer, Javier Lopez-Rios, Karine Rizotti, Robin Lovell-Badge, Dominique Bonnet, Ilaria Malanchi, Ander Abarrategi","doi":"10.1038/s41413-025-00500-6","DOIUrl":"10.1038/s41413-025-00500-6","url":null,"abstract":"<p><p>Endochondral ossification is a physiological process involving a sequential formation of cartilage and bone tissues. Classically, cartilage and bone formation have been considered independent processes at cellular level. However, the recently described multiple cell differentiation dynamics suggest that some bone cells are indeed the progeny of cartilage cells, or chondrocyte-derived osteoblasts. We hypothesized that the cartilage-to-bone phenotype transition is triggered by specific molecular events. First, the process was assessed in mouse bone tissue, and then, it was mimicked using in vivo cell implantation and in vitro serial differentiation protocols. Data indicates that cartilage cells transition to bone cell phenotype during postnatal physiological bone formation. This process can be reproduced using cartilage precursor cells coupled to specific implantation procedures or differentiation protocols. Gene expression profiling reveals that NOTCH, BMP and MAPK signaling pathways are relevant at the phenotype-switch, while the transcription factors Mesp1, Alx1, Grhl3 and Hmx3 are the feasible driver genes for chondrocyte-derived osteoblasts formation. Altogether, this report shows that endochondral ossification can be modeled using primary cell cultures and data indicate that this process is regulated by specific molecular events, previously described at skeleton morphogenesis during embryo development, and from now on also linkable to postnatal bone development and regeneration processes.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"19"},"PeriodicalIF":20.1,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12886771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149074","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":"Sialin-STAT3 axis regulates bone homeostasis in mice.","authors":"Xiaoyu Li, Lei Hu, Yifan Xu, Xue Wang, Zichen Cao, Ou Jiang, Jiawei Yao, Meijing Liu, Sihan Kong, Jinsong Wang, Xiaogang Wang, Songlin Wang","doi":"10.1038/s41413-025-00504-2","DOIUrl":"10.1038/s41413-025-00504-2","url":null,"abstract":"<p><p>Mitochondrial regulation in mesenchymal stem cells (MSCs) serves as a critical determinant of bone formation and skeletal homeostasis. While dietary nitrate and its transporter Sialin are implicated in systemic homeostasis, their specific roles in MSCs' function remain unclear. Here, we demonstrate that Sialin deficiency impairs MSCs' function and disrupts bone homeostasis. Gain- and loss-of-function studies reveal that Sialin localizes to the mitochondrial membrane and promotes osteogenic differentiation by maintaining mitochondrial bioenergetic integrity. Mechanistically, Sialin recruits pSTAT3^S727 to mitochondria, forming a functional complex that activates mitochondrial bioenergy and stabilizes bone remodeling. Notably, dietary nitrate restores Sialin expression in aged mice, thereby enhancing MSCs' function and preventing osteoporosis. Our findings identify a nutrient-responsive signaling axis-nitrate-Sialin-pSTAT3^S727-that promotes osteogenic differentiation via mitochondrial homeostasis, offering a potential therapeutic strategy for age-related osteoporosis.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"20"},"PeriodicalIF":20.1,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12887030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149075","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":"Single cell atlas decodes the molecular dynamics of scar repair after human rotator cuff tear.","authors":"Yiming Qin, Guang Yang, Tao Zhang, Yuying Yang, Liyang Wan, Tao Zhang, Linfeng Wang, Zhiyu Hu, Zhu Dai, Hongkang Zhou, Chengjun Li, Jianzhong Hu, Hongbin Lu","doi":"10.1038/s41413-025-00501-5","DOIUrl":"10.1038/s41413-025-00501-5","url":null,"abstract":"<p><p>Irreversible fibrotic scarring after rotator cuff tear (RCT) compromises the mechanical properties of the healing tendon, yet the underlying mechanisms remain poorly understood. Here, we analyzed the histological features of human RCT scars, characterized by disruption of tendon architecture, disorganized collagen fibrils, and imbalance in type I/III collagen ratios and fibril diameters. Using single-cell RNA sequencing of tendon stumps from patients with RCT, we deconvolved the cellular and molecular landscape of the fibrotic scarring microenvironment. Heterogenous pro-fibrotic subclusters were identified and validated to participate into scar formation, including tendon stem cell, senescent tenocyte, SOX9-driven pro-fibrotic macrophage, and pro-fibrotic endothelial cells undergoing endothelial-mesenchymal transition (EndoMT). Furthermore, we found that osteopontin and TGF-β signaling were key drivers of extracellular matrix deposition, and their blockade ameliorated fibrotic scarring after RCT. Collectively, our study dissected the dynamic scarring microenvironment in human RCT and highlights potential therapeutic targets for preventing pathological scar formation.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"17"},"PeriodicalIF":20.1,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12877062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123759","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":"Sulfated chitosan mitigates acute lung injury induced bone loss via immunoregulation.","authors":"Yongxian Liu, Luli Ji, Fuwei Zhu, Jiaze Yu, Dongao Huang, Jingyuan Cui, Xiaogang Wang, Jing Wang, Changsheng Liu","doi":"10.1038/s41413-025-00475-4","DOIUrl":"10.1038/s41413-025-00475-4","url":null,"abstract":"<p><p>Respiratory inflammatory diseases disrupt bone metabolism and cause pathological bone loss. The lung-bone axis is established in chronic diseases like asthma and cystic fibrosis but is less studied in acute lung injury (ALI), recently implicated in COVID-19-induced bone loss. This study examined the effects of LPS-induced ALI on bone phenotype and explored the role of 2-N, 6-O sulfated chitosan (26SCS) in mitigating pneumonia-induced bone loss via inflammatory response modulation. Our findings show that 26SCS effectively reaches bone tissue after oral administration. It promotes macrophage polarization to the M2 phenotype, alleviating immune cascade reactions and inhibiting osteoclast-mediated bone resorption. Increased M2 macrophages support type H vessel formation, enhancing inflammatory bone vascularization. These effects foster a favorable osteogenic microenvironment and mitigate ALI-induced bone loss. While dexamethasone is effective in reducing inflammation, it can aggravate ALI-induced bone loss. Our research offers a therapeutic strategy targeting the lung-bone axis for inflammation-induced bone loss.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":"18"},"PeriodicalIF":20.1,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12877068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123751","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}