Apoptosis最新文献

{"title":"The CXCL8-CXCR2 axis promotes M2 macrophage polarization in ovarian cancer via RASGRP4-mediated mTOR-STAT3 signaling.","authors":"Mi Ren, Ling-Ling Chen, Lin-Yin Jiang, Hui-Hui Yu, Hai-Zhou Ji","doi":"10.1007/s10495-025-02128-7","DOIUrl":"10.1007/s10495-025-02128-7","url":null,"abstract":"<p><p>This study aimed to investigate whether CXCL8-CXCR2 axis in regulating M2 macrophage polarization via RASGRP4 related signaling in ovarian cancer. Data from The Cancer Genome Atlas (TCGA) database was used to assess the correlation between CXCR2 expression and M2 macrophage infiltration. THP-1 human monocytic cells were utilized to analyze the effects of CXCL8 on RASGRP4 expression and M2 polarization. In vivo experiments were conducted using xenograft models to evaluate the impact of CXCL8 and RASGRP4 on tumor growth and macrophage polarization. Among the CXCR2 co-expressed genes, RASGRP4 showed the highest positive correlation with M2 macrophage infiltration in ovarian cancer. Higher expression of RASGRP4 is associated with poorer progression-free survival in patients with serous ovarian cancer. CXCR2 knockdown or inhibition (using SB225002) reduced IL-8-induced upregulation of RASGRP4 mRNA and protein in THP-1 cells. Additionally, PLCβ2 silencing attenuated IL-8-induced RASGRP4 expression. Knockdown of RASGRP4 in THP-1 cells reduced M2 polarization, while overexpression restored it. The CXCL8-CXCR2 axis further enhances M2 polarization through RASGRP4-mediated mTOR-STAT3 signaling. In xenograft ovarian tumor models, knockdown of CXCL8, CXCR2, or RASGRP4 reduced tumor growth and M2 macrophage infiltration. In summary, the CXCL8-CXCR2 axis promotes M2 macrophage polarization via RASGRP4-mediated mTOR-STAT3 signaling in ovarian cancer. Targeting this pathway may be a promising therapeutic strategy to reprogram tumor-associated macrophages and enhance treatment efficacy.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1839-1851"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of the NcRNA/ferroptosis axis in lung cancer: molecular mechanisms and potential therapeutic targets.","authors":"Mina Alimohammadi, Samaneh Kahkesh, William C Cho, Najma Farahani, Mahdi Farhadi Khoozani, Ahmadreza Zare, Amirreza Nejadheidari, Marzieh Ramezani Farani, Afsaneh Kheirmand Parizi, Fereshteh Asgharzadeh, Seyedeh Mahdieh Khoshnazar, Mehrdad Hashemi, Afshin Taheriazam, Kiavash Hushmandi","doi":"10.1007/s10495-025-02127-8","DOIUrl":"10.1007/s10495-025-02127-8","url":null,"abstract":"<p><p>Lung cancer, the second most diagnosed malignancy globally, remains the leading cause of cancer-related deaths due to its aggressive nature and limited treatment success. Ferroptosis, a unique form of regulated cell death, is characterized by iron-dependent lipid peroxidation and oxidative stress, distinct from apoptosis and necrosis. It plays a dual role in cancer by promoting cell death while being suppressed in tumor progression. This suppression allows cancer cells, including lung cancer cells, to evade destruction, contributing to the disease's malignancy. However, ferroptosis-inducing agents have shown promise in targeting cancer cells resistant to conventional therapies, positioning ferroptosis as a therapeutic avenue in oncology. Non-coding RNAs (ncRNAs) emerge as pivotal regulators in this axis. These molecules, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), modulate ferroptosis-related pathways by targeting key regulators like GPX4, SLC7A11, and ACSL4. For instance, miRNAs can downregulate SLC7A11, enhancing sensitivity to ferroptosis, while lncRNAs can stabilize or suppress pathways that prevent lipid peroxidation. CircRNAs, acting as molecular sponges, influence ferroptosis by modulating miRNA activity. The deregulation of these ncRNAs in lung cancer underscores their significance in the disease's pathogenesis and progression. Understanding the ncRNA-ferroptosis axis offers a novel perspective in addressing this challenge. Therapeutic strategies targeting this axis aim to selectively induce ferroptosis in tumor cells while sparing normal cells, enhancing treatment specificity and efficacy. Furthermore, combining ncRNA-based therapeutics with ferroptosis inducers provides a promising framework for overcoming drug resistance and improving outcomes. This review highlights comprehensive insight into the molecular mechanisms and therapeutic potential of the ncRNA-ferroptosis axis that could pave the way for more effective lung cancer treatments.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1665-1694"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mechanistic study of quercetin in the treatment of alcoholic brain injury via the JNK/P38 MAPK signaling pathway.","authors":"Yang Zhang, Binchuan Wang, Lisha Liu, Xu Huang, Yu Cai, Lishang Liao, Xuefeng Min, Yingjiang Gu","doi":"10.1007/s10495-025-02125-w","DOIUrl":"10.1007/s10495-025-02125-w","url":null,"abstract":"<p><p>Alcoholic brain damage (ABD) stems from chronic excessive alcohol consumption, causing neuroinflammation, oxidative stress, mitochondrial dysfunction, and neuronal apoptosis, all of which severely impair cognition and quality of life. However, traditional treatments have shown limited efficacy. Quercetin (QE), a natural flavonoid with antioxidant, anti-inflammatory, and neuroprotective properties, may therefore offer a promising approach for ABD. Accordingly, this study examines QE's potential mechanisms, with an emphasis on its modulation of the JNK/P38 MAPK pathway. In vitro, QE's effects on BV2 and HT22 cell viability were assessed via the CCK8 assay. Additionally, oxidative stress markers, including reactive oxygen species (ROS) and glutathione, were measured. Transmission electron microscopy was employed to observe cellular changes, while flow cytometry was used to evaluate apoptosis. Furthermore, western blotting was conducted to analyze the expression of BAX, Bcl-2, Caspase-3, IL-1, IL-6, TNF-α, P-P38, P-JNK, P38, and JNK. In vivo, SD rats were divided into a control group, an ethanol group, and three QE groups (25, 50, 100 mg/kg body weight), which were treated concurrently with ethanol for 12 weeks. Behavioral tests, histological staining, oxidative stress markers, and protein expression were examined. QE increased superoxide dismutase (SOD) activity, lowered ROS and malondialdehyde (MDA) levels, and reduced mitochondrial damage in vitro. It also significantly inhibited ethanol-induced apoptosis, inflammation, and JNK/P38 MAPK activation. Furthermore, QE improved spatial cognition, reduced anxiety, and ameliorated oxidative and inflammatory damage. Overall, QE alleviated alcohol-induced neuronal injury by suppressing oxidative stress, apoptosis, and inflammation via the JNK/P38 MAPK pathway, highlighting its therapeutic potential for ABD.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1875-1892"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polymeric immunoglobulin receptor (pIgR) in cancer progression: a critical role and potential therapeutic target.","authors":"Shaoju Qian, Yeqing He, Ruixue Li, Panpan Sun, Xingyi Zhang, Lin Pan, Zhishan Xu, Zhiwei Feng, Rong Lian, Lili Yu","doi":"10.1007/s10495-025-02116-x","DOIUrl":"10.1007/s10495-025-02116-x","url":null,"abstract":"<p><p>Polymeric immunoglobulin receptor (pIgR) is a crucial receptor that primarily mediates the transcytosis of immunoglobulins A and M across epithelial cells, emerging as an essential participant in modulating both mucosal immunity and innate immunity. Recently, pIgR dysregulation in cancer has garnered widespread attention. It exhibits distinct mechanisms and effects across various cancer types with significant clinical value as a biomarker for malignant tumor diagnosis and prognosis evaluation. Recent therapeutic advances have revealed promising strategies, including dimeric IgA-based approaches targeting intracellular oncogenic drivers through pIgR-mediated transcytosis, small molecule modulators such as bufalin, and targeting EV-pIgR with neutralizing antibodies. Integrating these approaches with conventional therapies presents opportunities for enhanced treatment efficacy. Specifically, blocking EV-pIgR with neutralizing antibodies, when integrated with conventional hepatocellular carcinoma therapies such as sorafenib or other therapeutic agents, or a dIgA-targeting approach combined with immune checkpoint inhibitors, may enhance treatment efficacy. This review also addresses current challenges and future directions in pIgR-targeted cancer therapy, emphasizing the need for a deeper understanding of pIgR's regulatory mechanisms. These insights reveal that pIgR is an emerging therapeutic target with significant potential for the development of novel cancer treatment strategies.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1751-1775"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144140979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel programmed cell death signature predicts clinical outcomes in clear cell renal cell carcinoma and identifies PLK1 as a therapeutic target.","authors":"Hao-Tian Tan, Chang-Yu Ma, Chong-Hao Sun, Shu-Zhan Sun, Ming-Xiao Zhang, Jian-Feng Wang","doi":"10.1007/s10495-025-02126-9","DOIUrl":"10.1007/s10495-025-02126-9","url":null,"abstract":"<p><p>Clear-cell renal cell carcinoma (ccRCC) remains therapeutically challenging despite recent treatment advances. Here, we analyzed 18 distinct programmed cell death (PCD) patterns across multiple cohorts and developed a novel prognostic scoring system (PCDscore) based on eight PCD-related genes. We established an eight-gene signature that demonstrated robust predictive capability and, when integrated with clinical staging, yielded a nomogram with strong performance across independent cohorts. High PCDscore groups exhibited enhanced immunosuppressive features, while low PCDscore groups showed better immunotherapy responses. Single-cell analysis of 54,166 cells revealed activation of multiple oncogenic pathways in high PCDscore tumor cells, along with extensive intercellular communication networks. To further investigate the role of PLK1, we identified 282 co-expressed genes and conducted functional enrichment analyses, revealing its significant association with pathways such as the cell cycle and NF-κB signaling. A protein-protein interaction (PPI) network and Bayesian network analysis highlighted PLK1 as a key regulator of PKMYT1, with CDC20 and CCNB2 acting upstream. Functional validation confirmed PLK1, the highest weighted gene in our signature, significantly influences tumor progression in ccRCC. This study establishes a reliable prognostic scoring system and identifies PLK1 as a potential therapeutic target, providing valuable clinical guidance for treatment decision-making in ccRCC patients.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1797-1825"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis: a novel therapeutic warrior in the battle against leukemia.","authors":"Yiduo Bai, Yizhi Luo, Yiyi Yuan, Xuan Li, Junchang Jin, Ruijing Ping, Jiuru Guo, Liuxu Jin, Yi Yu, Yuyan Xiong","doi":"10.1007/s10495-025-02130-z","DOIUrl":"10.1007/s10495-025-02130-z","url":null,"abstract":"<p><p>Ferroptosis is a newly discovered form of iron-dependent programmed cell death, characterized by the accumulation of lethal lipid peroxidation (LPO) driven by iron overload and dysregulated intracellular redox homeostasis. Leukemia, a heterogeneous group of malignant blood system tumors, typically manifests with increased oxidative stress and iron overload. A growing body of studies have revealed intimate interactions between ferroptosis and leukemia. Induction of ferroptosis has been demonstrated to mitigate the development and progression of leukemia, thus providing novel insights into potential therapeutic strategies for leukemia. In this review, we examine the characteristics and biological processes of ferroptosis, highlighting the action mechanisms of key ferroptosis-related regulators, including iron, glutathione (GSH), glutathione peroxidase 4 (GPX4), system X_c^-, lipid reactive oxygen species (ROS), p53, and mitochondria, in contributing to leukemia. This review also underscores the significant therapeutic potential of targeting ferroptosis in leukemia therapy using regulators such as system X_c^- inhibitors, GSH/GPX4 inhibitors, lipid ROS inducers, and natural compounds. Finally, we identify key unresolved questions and challenges that warrant further investigation in future translational studies.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1776-1795"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc ions trigger PANoptosis-like cell death in magnetic hyperthermia therapy of magnesium based implant for hepatocellular carcinoma.","authors":"Anhong Liu, Xiao Han, Qianqian Yang, Xiangxue Meng, Hao Qiu, Chunjie Wu, Xiaoming Li, Mengmeng Cai, Tinghe Duan, Zhanhui Wang","doi":"10.1007/s10495-025-02132-x","DOIUrl":"10.1007/s10495-025-02132-x","url":null,"abstract":"<p><p>The treatment of hepatocellular carcinoma (HCC) is a worldwide urgent and pressing challenge. Magnetic hyperthermia therapy (MHT) is a relatively new therapeutic strategy for tumors in resent years, especially magnesium (Mg) implants with eddy thermal effect can be employed for MHT to therapy tumor. PANoptosis is a new type of programmed cell death (PCD), driven by Caspases and RIPKs through the formation of PANoptosomes. In our early study, we discovered Zn²⁺ came from Zn-LDH@Mg implant could induce pyroptosis. In this work, we further demonstrate that Zn²⁺ comes from Zn-LDH@Mg implant can induce PANoptosis-like cell death in MHT to therapy H22 cells and tumors, verified by immunofluorescence staining, TUNEL staining, western blot assay, ELISA and transcriptomics analysis. This work is the first time to combine MHT and PANoptosis to therapy HCC, emphasizing the importance of materials design for MHT, and providing a useful foundation for materials design combined with PCD to treat tumors.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1826-1838"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing IFIT3 suppresses the EGFR/VEGF pathway and modulates SOCS1 to attenuate skin fibrosis in systemic sclerosis.","authors":"Xiangyang Huang, Yi Liu, Hangling Fu, Xia Rong, Yiheng Zhao","doi":"10.1007/s10495-025-02115-y","DOIUrl":"10.1007/s10495-025-02115-y","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is a life-threatening autoimmune disease characterized by progressive skin and organ fibrosis. Although interferon signaling is dysregulated in SSc, the role of interferon-induced proteins like IFIT3 in the skin fibrosis of SSC remains unclear. Here, we demonstrate that IFIT3 expression is significantly elevated (p < 0.01) in SSc fibroblasts and promotes fibrosis via SOCS1-dependent activation of the EGFR/VEGF axis. Silencing IFIT3 upregulated SOCS1 (p < 0.05), suppressed EGFR/VEGF (p < 0.01), and inhibited fibroblast proliferation/migration (p < 0.01). In a bleomycin-induced SSc model, IFIT3 knockdown ameliorated skin/lung collagen deposition and fibrosis (p < 0.05). Our findings reveal a novel mechanism whereby IFIT3 regulates EGFR and VEGF through down-regulating SOCS1 in SSc fibrosis, identifying IFIT3 as a novel therapeutic target for SSc.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1852-1874"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells.","authors":"Rui Li, Zhiyuan Wang, Yueyue Yujiang, Mengyuan Hu, Hongkun Zhao, Fei Yan","doi":"10.1007/s10495-025-02129-6","DOIUrl":"10.1007/s10495-025-02129-6","url":null,"abstract":"<p><p>Ferroptosis is a novel regulated cell death characterized by excessive membrane lipid peroxidation in an iron- and ROS-dependent manner, which is increasingly recognized for its role in tumor suppression and overcoming therapy resistance in various cancers. Induction of ferroptosis has been shown to sensitize cancer cells to chemotherapy, targeted therapy, and immunotherapy, thereby providing a novel strategy to tumor therapy. Peroxiredoxin 1 (PRDX1), an antioxidant enzyme, regulates redox homeostasis and is involved in tumor invasion, metastasis and prognosis. Increasing evidence suggests that PRDX1 is a negative regulator of ferroptotic cell death. Hence, regulating ferroptosis, via targeting PRDX1 and regulating PRDX1' function, holds promise for the treatment of tumors. In this review, we comprehensively summarized the regulatory of PRDX1 on ferroptosis and discussed the potential of PRDX1-mediated ferroptosis on tumor therapy, aiming to provide a distinct method for finding potential targets to enhance the effectiveness of ferroptosis-based tumor treament.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1645-1664"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-mediated triple drug delivery enhances apoptosis in pancreatic cancer cells.","authors":"Ruixia Zhang, Yongjie Zhang, Fei Hao, Zhengxing Su, Xing Duan, Xiangrong Song","doi":"10.1007/s10495-025-02131-y","DOIUrl":"10.1007/s10495-025-02131-y","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is one of the most common malignant tumors of the digestive tract. Gemcitabine (GEM) is a first-line chemotherapeutic agent for unresectable PC, but systemic distribution of the drug, drug resistance, and clinical side effects undermine its efficacy. This study utilized bone marrow mesenchymal stem cell-derived exosomes (BMSC-EXOs) as a delivery vehicle for a triple-drug combination (galectin-9 siRNA/DOGEM/indocyanine green) to improve synergistic therapy against PC. Galectin-9 siRNA, prodrug DOGEM, and ICG were loaded into BMSC-Exos by electroporation and vortexing to prepare nanoformulations (iEXO-DG-ICG). iEXO-DG-ICG had an average size of 132 ± 2.6 nm and its release rate in pH 6.0 medium was all faster than in pH 7.4 medium. The cytotoxicity of iEXO-DG-ICG against PANC-02 cells was stronger than free GEM both in vitro and in vivo. The protein expression of galectin-9 in tumor cells decreased by 79% after treatment with iEXO-DG-ICG, and the proportions of CD8⁺ T cells and IFN-γ⁺ CD8⁺ T cells increased while the proportions of Tregs decreased. The tumor inhibition rate of iEXO-DG-ICG was 90.3%. The present study successfully constructed a multimodal delivery system, designated iEXO-DG-ICG, using EXO derived from BM-MSCs as carriers. This system exhibited good tumor targeting and pH-responsive release characteristics. Both in vitro and in vivo studies confirmed that iEXO-DG-ICG significantly enhanced anti-tumor effects through the synergistic effect of chemotherapy, immunotherapy, and phototherapy. These findings provide a new strategy and a research foundation for the clinical treatment of pancreatic cancer.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":"1893-1911"},"PeriodicalIF":6.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}