STEM CELLS最新文献

{"title":"Dual roles of MAPK-mediated C/EBPβ phosphorylation in promoting maturation and suppressing EMT during hepatocyte differentiation from hESCs.","authors":"Shoupei Liu, Xiangting Cao, Haibin Wu, Shuai Zhang, Xueyan Zhang, Sen Chen, Huanhuan Shan, Weili Gu, Yongjian Zhou, Yuyou Duan","doi":"10.1093/stmcls/sxag016","DOIUrl":"10.1093/stmcls/sxag016","url":null,"abstract":"<p><p>Human embryonic stem cell (hESC)-derived hepatocytes (hEHs) display functional deficits, particularly impaired albumin secretion and ammonia metabolism, compared to primary human hepatocytes (PHHs). Here, we investigated the regulatory role of CCAAT/enhancer-binding protein beta (C/EBPβ) in hepatocyte maturation. Forced C/EBPβ expression enhanced hepatocyte functionality and upregulated hepatocyte-specific genes, while suppressing epithelial-mesenchymal transition (EMT) via downregulating canonical EMT markers. Mechanistically, CUT&Tag and luciferase reporter assays confirmed C/EBPβ directly bound to the promoter regions of CDH1 (E-cadherin) and CPS1 (carbamoyl phosphate synthetase 1). Co-immunoprecipitation identified an interaction between C/EBPβ and the MAPK pathway. RNA interference combined with Western blot analysis revealed that MAPK1-mediated phosphorylation of C/EBPβ at Thr-235 augmented its transactivation activity, accelerating hepatocyte maturation. Our findings establish C/EBPβ as a master regulator that coordinates transcriptional networks and post-translational modifications during hEHs maturation, providing novel insights for generating mature hepatocytes for disease modeling and regenerative medicine applications.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147626433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem cell therapies to modulate harmful immune responses in kidney disease: progress toward clinical validation.","authors":"Qifeng Ou, Fuxuan Li, Shengkun Wang, Ruixue Chen, Cuiqing Ma, Matthew D Griffin","doi":"10.1093/stmcls/sxag015","DOIUrl":"10.1093/stmcls/sxag015","url":null,"abstract":"<p><p>Stem cell therapies hold promise for halting or reversing kidney disease and improving kidney transplant (KTx) outcomes. One route to large-scale clinical application of stem cell therapies for kidney disease is through their capacity to modulate the balance between tissue injury and repair via crosstalk with other cells. Among the key disease-modulating effects of stem cells is their interaction with components of the immune system involved in harmful inflammation during acute kidney injury (AKI), chronic kidney disease (CKD) and complications of KTx. Extensive basic research demonstrates that stem cells employ diverse paracrine mechanisms to re-program immunological activities from pro-inflammatory/pro-fibrotic to anti-inflammatory/pro-repair. The therapeutic benefits of these effects are confirmed in many pre-clinical models of AKI, CKD and KTx for autologous and allogeneic stem cells including hematopoietic stem cells, mesenchymal stem cells, renal progenitor cells, and induced pluripotent stem cells. Nonetheless, translating these findings into therapeutic immunomodulatory cell products that improve the lives of those with kidney disease is highly challenging. The aims of this review are to: (a) Summarize recent insights into the common molecular and cellular mechanisms of immune-mediated tissue injury in kidney disease and KTx along with the types of stem therapies that have been developed to address them. (b) Critically evaluate the extent to which clinical trials of stem cell products have validated such effects in humans with kidney disease and KTx. (c) Identify key bottlenecks to the large-scale application of stem cell therapies to reduce the burden of kidney disease on patients and societies.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13199064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell barcoding reveals lineage-dependent outcomes in hiPSC cardiac differentiation.","authors":"Sogu Sohn, Daylin Morgan, Cody Callahan, Katelyn Dockery, Amy Brock, Janet Zoldan","doi":"10.1093/stmcls/sxag017","DOIUrl":"10.1093/stmcls/sxag017","url":null,"abstract":"<p><p>Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have potential applications in treating cardiovascular disease but are currently limited in their clinical translation. This can be attributed in large part to the complex molecular and cellular interactions that underly cardiac differentiation, with current differentiation approaches yielding heterogeneous outcomes due to inadequate understanding and control of these interactions. We hypothesize that clonal lineage-dependent responses to differentiation contribute to these heterogeneous outcomes, and as such cardiac differentiations can be improved by tracking and controlling for hiPSC clonal heterogeneity, a variable often overlooked in current differentiation approaches. \"Fate priming,\" wherein clonal lineage identity determines differentiation fate, has been demonstrated in other stem cell differentiation pathways. We investigated fate priming in hiPSC cardiac differentiation using the ClonMapper cell barcoding platform to label, track, and isolate distinct hiPSC lineages from the same cell line. We show that certain hiPSC lineages preferentially differentiate into hiPSC-CMs or non-CMs. After isolating lineages with apparent fate priming, we found significant differences in cardiac differentiation outcomes between these single-clone populations and heterogeneous, multi-clone hiPSC populations. These findings indicate that lineage identity influences hiPSC cardiac differentiation outcomes.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13213603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LARP7 enhances the potential of dental pulp stem cells to promote peripheral nerve repair.","authors":"Zihan Yang, Guanlin Qu, Xiping Wang, Li Wang, Lu Chen, Guiqiang Fu, Wenze Chen, Zitong Yang, Wenjing Li, Yuqiong Zhou, Jiacheng Jin, Linxi Zhou, Duohong Zou","doi":"10.1093/stmcls/sxag013","DOIUrl":"10.1093/stmcls/sxag013","url":null,"abstract":"<p><strong>Background: </strong>Peripheral nerve injuries (PNIs) present a persistent clinical challenge due to the intrinsically limited regenerative capacity of peripheral nerves. While dental pulp stem cells (DPSCs) exhibit significant neuroregenerative potential, their therapeutic efficacy is constrained by hostile microenvironments and inherent functional heterogeneity. Genetic modification may offer a promising strategy to enhance their therapeutic capabilities.</p><p><strong>Methods: </strong>DPSCs were induced toward neural lineage differentiation, and key gene candidates were identified through qRT-PCR. Lentiviral-mediated gene interference was performed to modulate target gene expression, followed by comprehensive analysis of differentiation outcomes using qRT-PCR, Western blotting, and immunofluorescence assays. RNA sequencing was employed to uncover associated signaling pathways, which were subsequently validated through pharmacological inhibition with specific inhibitors. The therapeutic efficacy of genetically engineered DPSCs was evaluated in a rat model of sciatic nerve crush injury, with neural regeneration quantitatively assessed via neuroelectrophysiological measurements and histological analyses.</p><p><strong>Results: </strong>LARP7 positively regulated the Schwann cell-like differentiation of DPSCs, as well as their trophic and anti-inflammatory effects, thus enhancing its therapeutic effects on nerve repair and promoting functional recovery. Mechanistically, we found that LARP7 remodeled cytokine-cytokine receptor interactions, enhancing trophic support while attenuating proinflammatory responses, and activated the PI3K-Akt-mTOR signaling pathway, with ERBB4 serving as a critical downstream effector, promoting DPSCs differentiation into Schwann cell-like phenotypes.</p><p><strong>Conclusions: </strong>Collectively, LARP7-mediated changes in DPSCs establish a new therapeutic paradigm that addresses the limitations of current stem cell-based interventions and enables the development of standardized biotherapeutics for peripheral nerve repair.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem cells enhance mitochondrial function in experimental Huntington's disease.","authors":"Francesco D'Egidio, Napasiri Putthanbut, Michaela Starahs, Jea Young Lee, Cesario V Borlongan","doi":"10.1093/stmcls/sxag019","DOIUrl":"10.1093/stmcls/sxag019","url":null,"abstract":"<p><p>Huntington's disease (HD) is a neurodegenerative disorder caused by cytosine-adenine-guanine (CAG) triplet expansion in the HTT gene, producing a mutant Huntingtin protein that impairs mitochondrial dynamics by reducing fusion and increasing fission. Mesenchymal stem cells (MSCs) have shown potential therapeutic effects by sharing functional mitochondria and other secretomes. In this study, quinolinic acid-lesioned neuro-2a (QA-N2a) cells and glutamatergic neurons with 50 CAG repeats (HD neurons) were co-cultured with human umbilical cord-derived MSCs for 5 hours. For QA-N2a cells, immunocytochemistry (ICC) was performed to demonstrate the change in GABA and Substance P before and after co-culture. For HD neurons, ICC was conducted to identify mitochondrial proteins, while Western blot was employed to evaluate proteins related to inflammation and mitochondrial function. As a result, co-culture with MSC significantly restored the expression of GABA and Substance P, which diminished after QA exposure. In HD neurons co-cultured with MSCs, an increase in mitochondrial abundance was observed, with significantly higher intensity and dendritic distribution of mitochondria compared to control cells. Western blot analysis confirmed this increase and showed a rising trend in ATP5a levels. MSCs also promoted mitochondrial fusion, indicated by higher levels of Mitofusin 2 (MFN2) and Mitochondrial Dynamin Like GTPase (OPA1), and a trend of reduction in the fission marker Dynamin-Related Protein (DRP1). Additionally, the co-culture led to a decreased trend in neuroinflammation markers IL-6, TNF-α, MMP9, and p-NFkB. Collectively, this study demonstrates that MSCs alleviate HD pathology by restoring the mitochondria activity and potentially suppressing inflammation in two different HD in vitro models.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147669353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mouse growth plate injury model identified contributions of Pdgfra and Pdgfrb cellular descendants to bony bar formation.","authors":"Zhao Li, Myles Zhou, Xin Xing, Beicheng Du, Mary Archer, Chunbao Rao, Manyu Zhu, Aaron W James","doi":"10.1093/stmcls/sxag014","DOIUrl":"10.1093/stmcls/sxag014","url":null,"abstract":"<p><strong>Background: </strong>Growth plate injuries in pediatric patients can lead to serious musculoskeletal complications, such as bony bar formation and potential growth arrest. Current clinical treatments have significant limitations, necessitating improved research models.</p><p><strong>Methods: </strong>The present study developed a highly reproducible drill-hole injury model in the mouse distal femur and introduces a quantitative scoring system for assessing bony bar formation. Using micro-computed tomography (μCT) and histological analyses, we evaluated bone tissue formation over a 42-day period. A 5-point grading system was developed to evaluate bony bar extent, validated through radiological and histological comparisons. We further examine the utility of the model by injuring either transgenic mice with lineage tracing for platelet-derived growth factor receptor alpha (Pdgfra) or beta (Pdgfrb).</p><p><strong>Results: </strong>we demonstrate a progressive increase in bone tissue formation over a 42-day period. While not present before injury, both Pdgfra and Pdgfrb reporter+ cells migrate into sites of growth plate injury and participate in bony bar formation.</p><p><strong>Conclusion: </strong>This model offers a standardized, reproducible, and validated approach to quantitatively study growth plate injury mechanisms, facilitating the use of transgenic animal models or the development of new therapeutic strategies in pediatric orthopedics.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147508206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicle microRNAs from human bone marrow MSCs suppress fibrogenesis of hepatic stellate cells by downregulation of RhoA signaling.","authors":"Daiki Kawamoto, Toshihiko Matsumoto, Tsuyoshi Fujioka, Shuhei Shinoda, Koichi Fujisawa, Tsuyoshi Ishikawa, Naoki Yamamoto, Taro Takami","doi":"10.1093/stmcls/sxag006","DOIUrl":"10.1093/stmcls/sxag006","url":null,"abstract":"<p><p>We have developed a liver regeneration therapy for decompensated liver cirrhosis (DLC) using autologous bone marrow mesenchymal stem cells (MSCs), and it is currently under trial (jRCT2063200014). However, the mechanism underlying the anti-fibrotic action of MSCs remains unclear. Therefore, we aimed to investigate the anti-fibrotic effects of microRNAs (miRNAs) in extracellular vesicles (EVs) derived from human bone marrow MSCs. We performed a comprehensive microarray analysis of miRNA expression profiles of MSC-EVs from healthy individuals, patients with DLC, and hepatic stellate cells (HSCs). We identified 11 miRNAs that showed a normalized intensity > 1000 in MSC-EVs, which was 50-fold higher than that in HSCs. MiRNA mimics for the 11 miRNAs were transfected into HSCs, and five miRNAs (miR-204-3p, miR-7977, miR-1237-5p, miR-5787, and miR-6089) that suppressed the expression of fibrosis-related genes (α-SMA, collagen I, and elastin) were identified. Transfection of the five-miRNA cocktail into HSCs decreased the expression of all fibrosis-related genes. Subsequently, pathway analysis revealed the downregulation of the RhoA signaling pathway, a key pathway in HSC activation. RhoA activity and migration were suppressed in HSCs transfected with the five-miRNA cocktail. This study identified five anti-fibrotic miRNAs enriched in MSC-EVs and elucidated the underlying mechanism of the anti-fibrotic action of MSCs.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146211801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Highly efficient induction of Sox9+ scl-progenitors from embryonic stem cells for skeletal modeling.","authors":"Yanhui Deng, Jingfei Xiong, Hanyi Chen, Runxin Ma, Weidong Tian, Yike Yin, Zhonghan Li","doi":"10.1093/stmcls/sxag007","DOIUrl":"10.1093/stmcls/sxag007","url":null,"abstract":"<p><p>Sclerotomal progenitors derived from pluripotent stem cells hold promises for modeling skeletal development and recapitulating the perinatal marrow niche that may provide insights into hematopoietic niche formation and immune regulation. Current strategy to derive mouse sclerotomal progenitors suffered from low differentiation efficiency and heterogeneous cell progenies. Here, we developed a fast and efficient strategy to generate sclerotomal progenitors by accelerated induction from primitive streak (PS) through modulating BMP and SHH signaling, achieving an 86.9% differentiation efficiency. Moreover, the resulting progenitors showed similar global gene expression profiles to those of the primary sclerotome, possessed strong osteochondral bipotential, and could recapitulate key features of endochondral ossification upon micromass-mediated osteogenic induction, including perinatal bone marrow (BM)-like niches regeneration. Our findings underscore accelerated sclerotomal induction from the primitive streak as an efficient strategy to derive sclerotomal progenitors for skeletal modeling and BM niche bioengineering.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146211774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prostaglandin E2 receptor EP2 is indispensable for maintenance of skeletal muscle stem cells.","authors":"Yusuke Maruyama, Ken'ichiro Nogami, Norio Motohashi, Fusako Sakai-Takemura, Ahmed Elhussieny, Fumiaki Uchiumi, Yoshitsugu Aoki, Shin'ichi Takeda, Yuko Miyagoe-Suzuki","doi":"10.1093/stmcls/sxag012","DOIUrl":"10.1093/stmcls/sxag012","url":null,"abstract":"<p><p>Muscle satellite cells are adult muscle stem cells indispensable for growth and regeneration of postnatal skeletal muscle. Notch plays a central role in maintenance of muscle satellite cells, but how Notch maintains the muscle stem cell pool is not fully understood. Previously, we reported that a prostaglandin E2 receptor, EP2, is upregulated by Notch signal and suppresses differentiation of human muscle progenitors. Here we examined the roles of EP2 in muscle satellite cells using a mouse Cre-LoxP conditional gene knockout system. Genetic inactivation of the EP2 gene (PTGER2) activated muscle satellite cells, caused their loss, and impaired muscle regeneration. These results indicate that EP2 is indispensable for maintenance of satellite cells. Ex vivo analysis using isolated myofibers showed that prostaglandin E2 (PGE2) delayed the activation of satellite cells via EP2. An extracellular signal-regulated kinase (ERK) 1/2 inhibitor blocked the activation of satellite cells on myofibers, and PGE2 attenuated the phosphorylation of ERK1/2 in muscle satellite cells. These results suggest that EP2 keeps the quiescence of satellite cells and maintains the satellite cell pool in part by inhibiting the ERK1/2 signaling pathway.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal stem cells derived EXO-miR3671 delivery promoted angiogenesis and accelerated wound healing of diabetes.","authors":"Jiannan Li, Sibing Chen, Huannan Wang, Wan Wang, Yanxi Liu","doi":"10.1093/stmcls/sxag008","DOIUrl":"10.1093/stmcls/sxag008","url":null,"abstract":"<p><strong>Objective: </strong>To explore the effect of exosomes-encapsulated miR3671 (EXO-miR3671) from mesenchymal stem cells (MSC) on diabetic wound healing and its mechanism.</p><p><strong>Methods: </strong>Bioinformatics analysis was conducted to identify gene and miRNA expression changes associated with diabetic foot ulcer (DFU). A diabetic mouse wound model was established, and dual-luciferase reporter assay was performed to verify the targeting relationship between miR3671 and QSOX1. For in vitro experiments, human umbilical vein endothelial cells (HUVECs) were cultured and transfected; the effects of EXO-miR3671 secreted by mesenchymal stem cells on HUVEC biological functions were detected via EdU proliferation assay, Transwell migration assay, and angiogenesis assay. For in vivo experiments, after dynamic measurement of wound areas in diabetic mice, HE staining, immunohistochemistry, and Western blot were employed to evaluate the regulatory effects of mesenchymal stem cell-derived EXO-miR3671 on wound healing process and related protein expression levels.</p><p><strong>Results: </strong>MiR3671 was downregulated in DFU tissues and diabetic mouse wounds. EXO-miR3671 promoted HUVEC proliferation, migration, and angiogenesis in vitro. In diabetic mice, it accelerated wound closure, reduced inflammation, increased Ki67+ cell proliferation, and upregulated pro-angiogenic growth factors.</p><p><strong>Conclusions: </strong>MSC-derived EXO-miR3671 could be a potential treatment for diabetic wounds, providing new insights for treatment.</p>","PeriodicalId":231,"journal":{"name":"STEM CELLS","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146211799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}