Experimental cell research最新文献

{"title":"Deciphering the role of circulating miRNAs in the etiology and pathophysiology of endometriosis: An updated compiled review","authors":"Anuja Pant ,&nbsp;Kareena Moar ,&nbsp;Taruna K. Arora ,&nbsp;Tikam Chand Dakal ,&nbsp;Vipin Ranga ,&nbsp;Narendra Kumar Sharma ,&nbsp;Pawan Kumar Maurya","doi":"10.1016/j.yexcr.2025.114482","DOIUrl":"10.1016/j.yexcr.2025.114482","url":null,"abstract":"<div><div>Endometriosis is characterized by the presence of endometrial tissue outside of the uterus. It is a benign chronic condition with incapacitating symptoms like infertility and pelvic pain. Endometriosis has a detrimental impact on the reproductive health of women, placing a heavy financial strain on the medical system. It is a multifactorial disorder governed by numerous mechanisms or risk factors that contribute to the pathologies of the disease. With limitations in diagnostics techniques, it is challenging to detect the disease at an initial stage. In around 1 % of endometriotic patients malignant state may reach, leading to severe consequences. To overcome such challenges, at present, numerous circulating miRNAs have been studied in plasma or serum samples from patients with endometriosis to develop a non-invasive diagnostic biomarker-based tool to identify the disease early. Our review compiles the miRNAs in bodily fluids that are linked with endometriosis-related mechanisms, which may serve as a potential biomarker. Some of these mechanisms are common in both cancer and endometriosis. Additionally, we have also emphasised the miRNAs with a putative role in cancer development and progression that could be used as a biomarker. This may further aid in protecting the 1 % of affected females from ovarian, breast, and in some cases endometrial cancer. We have come across several miRNAs associated with multiple mechanisms associated with endometriosis. miR-199a and miRNAs-let-7 family are some of the most common miRNAs that assist in multiple mechanisms such as cell proliferation, invasion, apoptosis, and epithelial-mesenchymal transition. Strategic planning and additional investigation into the identified miRNAs would make them a viable therapeutic target for the optimal management of endometriosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114482"},"PeriodicalIF":3.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143519219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing of LOX-1 attenuates high glucose-induced ferroptosis in THVECs via the HIF-1α/SLC7A11 signaling pathway","authors":"Haiqi Zhang ,&nbsp;Xinying Chang ,&nbsp;Xuan Liu ,&nbsp;Baozhuan Zhang ,&nbsp;Rongrong Wang ,&nbsp;Yuhui Wang ,&nbsp;Simeng Dai ,&nbsp;Tonghan Yao ,&nbsp;Qi Zhang","doi":"10.1016/j.yexcr.2025.114451","DOIUrl":"10.1016/j.yexcr.2025.114451","url":null,"abstract":"<div><h3>Objectives</h3><div>Diabetic osteoporosis (DOP) represents a significant and serious complication associated with diabetes, characterized by a complex and inadequately understood pathophysiological mechanism. Recent studies have highlighted a robust association between DOP and ferroptosis. H-type vessels play a critical role in osteoporosis, while lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is associated with endothelial dysfunction related to diabetes. In this study, we investigate how LOX-1 affects ferroptosis in H-type vascular endothelial cells (THVECs) under high glucose (HG) conditions, aiming to elucidate the molecular mechanisms involved.</div></div><div><h3>Methods</h3><div>THVECs were isolated from rats employing an enzymatic digestion method and subsequently validated through immunofluorescence analysis. The silencing of LOX-1 was achieved via transfection with a lentiviral vector. Cell viability was assessed using the CCK-8 assay, and ROS, MMP, GSH, MDA, and Fe²⁺ levels were assessed utilizing specific commercial kits. Western blotting and PCR assessed LOX-1, HIF-1α, SLC7A11, and GPX4 expression levels.</div></div><div><h3>Results</h3><div>In high glucose conditions, LOX-1 expression at both protein and mRNA levels increased, while ROS, MDA, and Fe²⁺ rose, and MMP and GSH levels fell, resulting in ferroptosis in THVECs. This condition could be reversed by silencing LOX-1 or by administering the ferroptosis inhibitor (Fer-1). Further analysis showed that silencing LOX-1 enhanced the expression of HIF-1α, SLC7A11, and GPX4, which mitigated ferroptosis in THVECs.</div></div><div><h3>Conclusions</h3><div>Downregulation of LOX-1 alleviates high glucose-induced ferroptosis in THVECs via the HIF-1α/SLC7A11 pathway. This suggests that LOX-1 functions as a critical target for regulating ferroptosis in THVECs, providing a novel insight into the pathological mechanisms associated with DOP.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114451"},"PeriodicalIF":3.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A m6A writer RBM15 enhances the cell malignancy of osteosarcoma by mediating m6A modification of lncRNA THAP9-AS1","authors":"Hao Zou ,&nbsp;Fei Hu ,&nbsp;Xin Wu ,&nbsp;Bin Xu ,&nbsp;Guifeng Shang ,&nbsp;Dong An ,&nbsp;Dehao Qin ,&nbsp;Xiaolei Zhang ,&nbsp;Aofei Yang","doi":"10.1016/j.yexcr.2025.114490","DOIUrl":"10.1016/j.yexcr.2025.114490","url":null,"abstract":"<div><h3>Background</h3><div>Osteosarcoma (OS) remains a potentially fatal disease in children. Increasing evidence highlights the implication of lncRNAs and N6-methyladenosine (m6A) modification in OS malignancies. Here, we aimed to decipher the pathological significance of RBM15-mediated m6A modification of lncRNA THAP9-AS1 in OS progression.</div></div><div><h3>Methods</h3><div>The expression levels of THAP9-AS1 and RBM15 in OS tissues and cell lines was determined by qRT-PCR. Based on the abnormal regulation of THAP9-AS1 and RBM15, the CCK8, colony-formation, and transwell invasion assays were used to evaluate the viability, clone formation capacity, and invasive ability of OS cells. A mouse model of tumor transplantation was utilized to ascertain the role of THAP9-AS1 silencing <em>in vivo</em>. The relationship between THAP9-AS1 and RBM15 was determined by RIP and MeRIP assays.</div></div><div><h3>Results</h3><div>THAP9-AS1 and RBM15 were significantly elevated in OS. Silencing of THAP9-AS1 or RBM15 decreased the proliferative and invasive ability of OS cells <em>in vitro</em>, and inhibition of THAP9-AS1 delayed the tumorous growth <em>in vivo</em>. Interestingly, THAP9-AS1 binds to RBM15, and was stimulated by RBM15 to promote m6A level and translation. Furthermore, THAP9-AS1 upregulation promoted OS cell invasion and survival, and this promotion of OS cell malignancy was abrogated by RBM15 silencing.</div></div><div><h3>Conclusion</h3><div>THAP9-AS1 serves as a tumor promoter by accelerating the malignant progression of OS by undergoing m6A modification, which is mediated by RBM15. This suggests that RBM15-m6A-THAP9-AS1 may be a potential target for OS treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114490"},"PeriodicalIF":3.3,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel strategy for hair regeneration: Exosomes and collagenous sequences of human a1(XVII) chain enhance hair follicle stem cell activity by regulating the hsa-novel-238a-CASP9 axis","authors":"Jingyu Zhao ,&nbsp;Zhe Quan ,&nbsp;Huiying Wang ,&nbsp;Jun Wang ,&nbsp;Yong Xie ,&nbsp;Jiajia Li ,&nbsp;Ruzhi Zhang","doi":"10.1016/j.yexcr.2025.114483","DOIUrl":"10.1016/j.yexcr.2025.114483","url":null,"abstract":"<div><div>The regenerative capacity of hair follicles is fundamentally influenced by the intricate interactions between hair follicle stem cells (HFSCs) and their microenvironment. Our study presents a novel strategy for hair regeneration, highlighting the synergistic relationship between dermal papilla cell-derived exosomes (DPC-Exos) and collagenous sequences of Human a1(XVII) Chain (CS-COL17A1) in modulating HFSC activity via the hsa-novel-238a-CASP9 axis. We characterized DPC-Exos using nanoparticle tracking analysis and transmission electron microscopy and confirmed, their purity with the exosomal markers CD81, CD63, and CD9.A dose-dependent CCK-8 assay showed that both DPC-Exos and CS-COL17A1 significantly improved HFSC viability. Scratch and Transwell assays showed improved HFSC migration after treatment. MiRNA sequencing revealed a significant upregulation of hsa-novel-238a in HFSCs after treatment with DPC-Exos and CS-COL17A1, suggesting its involvement in the regulation of HFSCs activity. A dual-luciferase assay confirmed that hsa-novel-238a directly targets the CASP9 gene, elucidating the underlying molecular mechanisms. The combined application of DPC-Exos and CS-COL17A1 significantly improved HFSC migration and proliferation (p &lt; 0.01), highlighting the importance of the hsa-novel-238a-CASP9 axis. This research provides insights into the regulatory network of exosomes and CS-COL17A1, paving the way for innovative therapeutic approaches to treat hair loss and enhance hair follicle regeneration through modulation of the hsa-novel-238a-CASP9 axis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114483"},"PeriodicalIF":3.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasmin reduces human T cell arrest on endothelial-like cells by cleaving bound CCL21 from the cell surface","authors":"James Jack Willis Hucklesby ,&nbsp;Catherine Elizabeth Angel ,&nbsp;Euan Scott Graham ,&nbsp;Peter Rod Dunbar ,&nbsp;Nigel Peter Birch ,&nbsp;Evert Jan Loef","doi":"10.1016/j.yexcr.2025.114480","DOIUrl":"10.1016/j.yexcr.2025.114480","url":null,"abstract":"<div><div>CCL21 is a key homeostatic chemokine best known for its role in lymphocyte homing and compartmentalization in the lymph node. CCL21 also plays a role in trans-endothelial migration and is known to be bound to the surface of endothelial cells in high endothelial venules and inflamed tissues. The effects of CCL21 are highly dependent on its form; full-length CCL21 can bind to the surface of endothelial cells and induce lymphocyte arrest and transendothelial migration, whereas truncated CCL21 cannot. Earlier literature indicates that plasmin can cleave CCL21 from the surface of immune cells, although the mechanism regulating this process on endothelial cells has not been studied.</div><div>This study demonstrates that the human endothelial-like cell lines ECV304 (LS12) and HMEC-1 can bind the plasmin precursor plasminogen to their cell surface. Furthermore, ECV304 (LS12) cells could endogenously activate plasminogen, yielding plasmin that subsequently released cell surface CCL21. In contrast, cell-surface CCL21 was only released from HMEC-1 after exogenous tPA activated the surface-bound plasminogen. Finally, it was shown that plasmin reduced T cell adhesion to endothelial-like cells with cell surface CCL21 under shear stress conditions.</div><div>Collectively, for the first time, these data demonstrate that plasmin can cleave endothelial cell surface CCL21, reducing T cell adhesion to endothelial cells under shear stress. Interestingly, this study also indicates that endothelial cells’ differential expression of plasminogen activators may regulate plasmin availability and influence T-cell arrest.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114480"},"PeriodicalIF":3.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactate promotes the epithelial-mesenchymal transition of liver cancer cells via TWIST1 lactylation","authors":"Wang Huimin ,&nbsp;Wu Xin ,&nbsp;Yu Shan ,&nbsp;Zhang Junwang ,&nbsp;Wen Jing ,&nbsp;Wang Yuan ,&nbsp;Liu Qingtong ,&nbsp;Li Xiaohui ,&nbsp;Yao Jia ,&nbsp;Yuan Lili","doi":"10.1016/j.yexcr.2025.114474","DOIUrl":"10.1016/j.yexcr.2025.114474","url":null,"abstract":"<div><div>Elevated lactate levels increase the risk of liver cancer progression. However, the mechanisms by which lactate promotes liver cancer progression remain poorly understood. Epithelial-mesenchymal transition (EMT), characterized by the loss of epithelial cells polarity and cell-cell adhesion, leading to the acquisition of mesenchymal-like phenotypes, is widely recognized as a key contributor to liver cancer progression. TWIST1 (Twist Family BHLH Transcription Factor 1) plays a central role in inducing EMT. Here, we investigated the role of lactate in promoting EMT in liver cancer and the underlying regulatory mechanisms. High levels of lactate significantly promoted EMT progression in liver cancer cells. Mechanistically, lactate-induced lactylation of TWIST1 <em>in vivo</em> and <em>in vitro</em>. Mutation assay confirmed that Lysine 33 (K33) is the major site of TWIST1 lactylation. Moreover, cell fractionation &amp; luciferase reporter assay results identified that TWIST1-K33R mutant impaired the EMT process via inhibiting nuclear import and the transcriptional activity. Thus, our findings provide novel insights into the regulatory role of lactate in EMT in liver cancer pathogenesis. Additionally, targeting of lactate-driven lactylation of TWIST1 may boost the therapeutic strategy for liver cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114474"},"PeriodicalIF":3.3,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical stretch promotes the migration of mesenchymal stem cells via Piezo1/F-actin/YAP axis","authors":"Ning Ma ,&nbsp;Lei Huang ,&nbsp;Qianxu Zhou ,&nbsp;Xiaomei Zhang ,&nbsp;Qing Luo ,&nbsp;Guanbin Song","doi":"10.1016/j.yexcr.2025.114461","DOIUrl":"10.1016/j.yexcr.2025.114461","url":null,"abstract":"<div><div>Mesenchymal stem cells (MSCs) have self-renewal ability and the potential for multi-directional differentiation, and their clinical application has promising prospects, but improving the migration ability of MSCs <em>in vivo</em> is one of the challenges. We previously determined mechanical stretch at 1 Hz with 10 % strain for 8 h can significantly promote MSC migration, however, the molecular mechanism remains poorly understood. Here, we reported that the expression and activity of yes-associated protein (YAP) are upregulated after mechanical stretch. As a classical inhibitor of the YAP-TEAD activity and YAP protein, the treatment of verteporfin (VP) suppressed mechanical stretch-promoted MSC migration. We also observed F-actin polymerization after mechanical stretch. Next, we used Latrunculin A (Lat A), the most widely used reagent to depolymerize actin filaments, to treat MSCs and we found that Lat A treatment inhibits MSC migration by suppressing YAP expression and activity. In addition, the protein expression of Piezo1 was also upregulated after mechanical stretch. Knockdown of Piezo1 suppressed mechanical stretch-promoted MSC migration by restraining F-actin polymerization. Together, these findings demonstrate the role of Piezo1/F-actin/YAP signaling pathway in MSC migration under mechanical stretch, providing new experimental evidence for an in-depth understanding the mechanobiological mechanism of MSC migration.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114461"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the initial effects of carcinogen-induced oncogenic transformation in the mouse bladder","authors":"Md. Kaykobad Hossain ,&nbsp;Lucas Unger ,&nbsp;Ulrik Larsen ,&nbsp;Altanchimeg Altankhuyag ,&nbsp;Thomas Aga Legøy ,&nbsp;Joao A. Paulo ,&nbsp;Heidrun Vethe ,&nbsp;Luiza Ghila","doi":"10.1016/j.yexcr.2025.114452","DOIUrl":"10.1016/j.yexcr.2025.114452","url":null,"abstract":"<div><div>Characterizing the initial stages of oncogenic transformation allows the identification of tumor-promoting processes before the inherent clonal selection of the aggressive clones. Here, we used global proteomics, genetic cell tracing, and immunofluorescence to dynamically map the very early stages of cancer initiation in a mouse model of bladder cancer. We observed a very rapid and incremental proteome dysregulation, with changes in the energy metabolism, proliferation and immune signatures dominating the landscape. The changes in the lipid metabolism were immediate and defined by an increase fatty acid metabolism and lipid transport, followed by the activation of the immune landscape. Alongside the changes in the immune signature and lipid metabolism, we also mapped a clear increase in the cell cycle-related pathways and proliferation. Proliferation was mainly restricted to the basal epithelial layer rapidly leading to urothelium thickening, despite the progressive loss of the superficial layer. Moreover, we observed a tilt in the energy balance towards increased glucose metabolism, probably characterizing cells of the tumor microenvironment. All of the observed proteome signature changes were persistent, being retained and sometimes intensified or diversified along the timeline. The signatures observed in this pilot suggest these processes as potentially targetable drivers of the future neoplastic transformations in the bladder.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114452"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activated NETosis of bone marrow neutrophils up-regulates macrophage osteoclastogenesis via cGAS-STING/AKT2 pathway to promote osteoporosis","authors":"Yutong Guo ,&nbsp;Hanzhang Zhou ,&nbsp;Yixiang Wang ,&nbsp;Yan Gu","doi":"10.1016/j.yexcr.2025.114477","DOIUrl":"10.1016/j.yexcr.2025.114477","url":null,"abstract":"<div><div>Bone marrow (BM) of postmenopausal osteoporosis has been found highly inflammatory, resulting from dysregulated immune cells induced by both estrogen efficiency and body aging. NETosis of neutrophils has been found aberrantly activated in age-related chronic inflammation, while their role in postmenopausal osteoporosis remains unclear. Here we found NETosis of BM neutrophils of OVX (ovariectomy) mice was significantly activated, and we verified NETs released by neutrophils induced M1 polarization and osteoclastogenesis of RAW264.7 macrophages. Further, we demonstrated effects of NETs on osteoclastogenesis was mediated by cGAS-STING/AKT2 pathway. Finally, we found <em>in vivo</em> NETs-clearance through GSK484 significantly inhibited osteoclastogenesis and attenuated osteoporosis of OVX mice. Our study highlights the role of neutrophil NETosis in activating osteoclastogenesis and bone resorption of postmenopausal osteoporosis, thereby providing novel targets for bone loss treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114477"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epic, classic, and remarkable: 75 years of Experimental Cell Research","authors":"Ji-Long Liu (Editor-in-Chief)","doi":"10.1016/j.yexcr.2025.114447","DOIUrl":"10.1016/j.yexcr.2025.114447","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114447"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}