Apoptosis最新文献

{"title":"KRAS-mediated CCDC6 degradation drives xCT upregulation and ferroptosis evasion","authors":"Daniela Criscuolo,&nbsp;Rosaria Catalano,&nbsp;Carmela Baviello,&nbsp;Claudia Fioravanti,&nbsp;Elena Vigliar,&nbsp;Francesco Morra,&nbsp;Maria Marotta,&nbsp;Junsei Mimura,&nbsp;Antonino Iaccarino,&nbsp;Francesco Pepe,&nbsp;Dorina Belotti,&nbsp;Giancarlo Troncone,&nbsp;Francesco Merolla,&nbsp;Rosa Marina Melillo,&nbsp;Angela Celetti","doi":"10.1007/s10495-026-02400-4","DOIUrl":"10.1007/s10495-026-02400-4","url":null,"abstract":"<div><p>Oncogenic KRAS mutations drive tumorigenesis by promoting pro-survival signaling and metabolic reprogramming, including the maintenance of redox balance to evade oxidative stress. A key mechanism involves the upregulation of the xCT cystine/glutamate antiporter, which sustains glutathione (GSH) synthesis and protects cells from oxidative damage and ferroptosis. While it is known that the ETS1-ATF4 complex mediates transcriptional upregulation of xCT, the upstream regulators linking KRAS signaling to this axis remain to be fully defined. Here, we demonstrate that oncogenic KRAS signaling induces the GSK3β-mediated proteasomal degradation of the tumor suppressor CCDC6. We show that CCDC6 acts as a negative regulator of the xCT-promoting transcription factor ATF4 by directly interacting with it and preventing its recruitment to the xCT promoter. Consequently, KRAS-driven CCDC6 degradation disinhibits ATF4, leading to increased xCT expression, elevated intracellular GSH, and enhanced resistance to ferroptosis. Crucially, pharmacological inhibition of CCDC6 turnover using proteasome, GSK3β, or specific KRAS mutant inhibitors (Sotorasib, Adagrasib, HRS4642) restored CCDC6 protein levels and robustly sensitized KRAS-mutated cells to ferroptosis-inducing agents like Sulfasalazine. Furthermore, validation in preclinical models and human colorectal cancer samples revealed that CCDC6 protein levels are predominantly downregulated in KRAS-mutant cases. This work uncovers a novel KRAS/CCDC6/xCT signaling axis that mediates ferroptosis resistance in KRAS-mutated cancers. Moreover, it identifies CCDC6 turnover as a critical vulnerability and a promising therapeutic target to enhance the efficacy of ferroptosis-inducing agents.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 8","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-026-02400-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148434005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Expression of Concern: N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production","authors":"Srabanti Rakshit,&nbsp;Jayashree Bagchi,&nbsp;Labanya Mandal,&nbsp;Kausik Paul,&nbsp;Dipyaman Ganguly,&nbsp;Sandip Bhattacharjee,&nbsp;Monidipa\t Ghosh,&nbsp;Nabendu Biswas,&nbsp;Utpal Chaudhuri,&nbsp;Santu Bandyopadhyay","doi":"10.1007/s10495-026-02397-w","DOIUrl":"10.1007/s10495-026-02397-w","url":null,"abstract":"","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 8","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418138","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":"GLI2 confers ferroptosis resistance in bladder cancer by transcriptionally upregulating PRDX1","authors":"Yuyang Yao,&nbsp;Pang Yang,&nbsp;Shaorui Niu,&nbsp;Jun Yang,&nbsp;Xiaofeng Tang,&nbsp;Wei Bai,&nbsp;Kangming Chen,&nbsp;Yuntong Zhou,&nbsp;Xiaorong Yang,&nbsp;Xiao-Bin Lv","doi":"10.1007/s10495-026-02395-y","DOIUrl":"10.1007/s10495-026-02395-y","url":null,"abstract":"<div><p>Bladder cancer represents a significant disease burden in men, as it is both highly common and a leading cause of cancer-related deaths. Despite advances in personalized therapies, patient outcomes continue to show considerable variability, and there is an urgent need to explore novel therapeutic targets for this disease. Ferroptosis has recently been implicated in chemotherapy response and proposed as a therapeutic target in various cancers; however, its regulatory mechanism in bladder cancer cells has not been fully elucidated. In this study, we analyzed public data from the GEO database and found that the transcription factor GLI2 was significantly upregulated in bladder cancer compared with normal bladder tissues. Functional assays revealed that GLI2 promotes malignant progression and represses ferroptosis in bladder cancer cells. Mechanistically, RNA sequencing and chromatin immunoprecipitation (ChIP) assays showed that GLI2 transcriptionally regulates the expression of peroxiredoxin 1 (PRDX1), a well-characterized ferroptosis-inhibiting gene. Additionally, rescue assay results indicated that PRDX1 mediates the role of GLI2 in ferroptosis repression and promotes malignant progression of bladder cancer. More importantly, inhibition of GLI2 via siRNA or a small-molecule inhibitor sensitized bladder cancer cells to both PRDX1 inhibitors and cisplatin. Together, these findings delineate a regulatory axis involving GLI2-PRDX1-mediated ferroptosis, provide mechanistic insights into its critical role in driving bladder cancer progression and chemosensitivity, and offer potential therapeutic targets for future clinical intervention.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 8","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418174","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":"Editorial Expression of Concern: JNK mediates UVB-induced apoptosis upstream lysosomal membrane permeabilization and Bcl-2 family proteins","authors":"Cecilia Bivik,&nbsp;Karin Öllinger","doi":"10.1007/s10495-026-02396-x","DOIUrl":"10.1007/s10495-026-02396-x","url":null,"abstract":"","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 8","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418103","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":"Axitinib promotes stemness and vasculogenic mimicry in triple-negative breast cancer by disrupting THBS1-CD47 axis-mediated endothelial-tumor cell communication","authors":"Lei Lei,&nbsp;Huanhuan Zhou,&nbsp;Xiaojing Lai,&nbsp;Zeng Wang,&nbsp;Rongguo Li,&nbsp;Chengyong Du,&nbsp;Xiangming He,&nbsp;Lingbin Du,&nbsp;Yabing Zheng,&nbsp;Xiaojia Wang,&nbsp;Xiying Shao","doi":"10.1007/s10495-026-02388-x","DOIUrl":"10.1007/s10495-026-02388-x","url":null,"abstract":"<div><p>Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic options. Although anti-angiogenic agents like Axitinib are used in cancers, resistance emerges through poorly understood mechanisms involving stemness and vasculogenic mimicry (VM). Here, we investigated the regulatory role of thrombospondin-1 (THBS1), an anti-angiogenic protein, in Axitinib-mediated signaling and its impact on TNBC. The effects of Axitinib on VM, angiogenesis, and stemness in TNBC were investigated through in vivo models and in vitro endothelial-supernatant cultures. Bioinformatics analyses (GSE230643 and CellChat), immunohistochemistry of clinical samples, exosome transfer assays, and xenograft models were employed to explore how Axitinib regulates THBS1-mediated endothelial-TNBC intercellular communication. Further bioinformatics analyses, combined with in vitro and in vivo experimental validations, were performed to elucidate the mechanism of the THBS1-CD47 axis in TNBC. Axitinib treatment increased stemness and promoted VM in TNBC models, despite tumor growth inhibition. Bioinformatics analyses revealed the Axitinib-dependent THBS pathway between endothelial and endothelial-like tumor cells. Axitinib-induced downregulation of THBS1 expression in HUVEC cells promoted stemness and angiogenesis of recipient TNBC cells via exosomes. Mechanistically, endothelial-derived THBS1 promoted CD47 expression in recipient TNBC cells, thereby attenuating the activity of PI3K/Akt and MAPK/ERK signaling pathways, and inhibiting stemness, angiogenesis, and VM. Importantly, Axitinib disrupted this THBS1-CD47 axis by downregulating endothelial-derived THBS1 expression. Axitinib induces the suppression of THBS1 expression in endothelial cells, thereby enhancing stemness and VM in recipient TNBC via disruption of the THBS1-CD47 axis. Restoring THBS1 signaling may represent a promising strategy to overcome Axitinib resistance.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 8","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-026-02388-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anoikis in cancer: molecular mechanisms, resistance, and therapeutic strategies","authors":"Zhihan Lin,&nbsp;Jiayi Wu,&nbsp;Huazhong Liu","doi":"10.1007/s10495-026-02402-2","DOIUrl":"10.1007/s10495-026-02402-2","url":null,"abstract":"<div><p>Anoikis is a programmed cell death pathway triggered by cell detachment from the extracellular matrix, playing an essential role in maintaining tissue homeostasis and preventing aberrant cell colonization. The acquisition of anoikis resistance by tumor cells is a prerequisite for distant metastasis and a major contributor to therapeutic failure in cancer treatment. This review systematically summarizes the molecular mechanisms governing anoikis and the core pathways through which tumor cells evade this form of cell death. The precise regulation of anoikis depends on the integration of apoptotic signals by Bcl-2 family proteins, which orchestrate three major signaling axes, the extrinsic death receptor pathway, the intrinsic mitochondrial pathway, and the caspase-independent pathway. Tumor cells develop resistance to anoikis through diverse mechanisms, including epithelial-mesenchymal transition (EMT), remodeling of the tumor microenvironment, concentration-dependent modulation by reactive oxygen species (ROS), autophagy and metabolic reprogramming, coordinated activation of multiple signaling cascades, and regulatory networks involving non-coding RNAs. Furthermore, this review discusses current therapeutic strategies targeting anoikis resistance, including combination therapy, gene therapy, and targeted therapy, and outlines future research directions. A deeper understanding of the molecular networks and regulatory mechanisms underlying anoikis resistance will provide a theoretical foundation for developing novel interventional strategies to counteract tumor metastasis.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 8","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418192","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":"Mitochondrial dysfunction and cellular senescence drive accelerated gestational aging in spontaneous preterm birth: a narrative review","authors":"Gagana Hanumaiah,&nbsp;Thejesh Srinivas,&nbsp;Akhila Vasudeva","doi":"10.1007/s10495-026-02394-z","DOIUrl":"10.1007/s10495-026-02394-z","url":null,"abstract":"<div><p>Spontaneous preterm birth (sPTB) is a leading cause of neonatal mortality and long-term morbidity worldwide, affecting approximately 15 million infants annually. Despite advances in obstetric care, its incidence has remained largely unchanged, reflecting an incomplete understanding of the biological mechanisms governing the timing of parturition. While infection and inflammation have traditionally dominated etiological models, these alone do not fully explain the heterogeneity in disease onset, progression, and outcomes. Emerging evidence suggests that sPTB may represent a state of accelerated gestational aging, in which cellular stress pathways prematurely activate labour mechanisms that are normally tightly regulated at term. This narrative review synthesizes current evidence linking mitochondrial dysfunction, oxidative stress, and cellular senescence to the pathogenesis of sPTB. Across gestational tissues, including the placenta, fetal membranes, decidua, cervix, and myometrium, molecular stress induces shifts characterized by impaired mitochondrial oxidative phosphorylation, increased reactive oxygen species generation, and activation of senescence-associated pathways. Beyond reflecting cellular injury, these processes actively propagate inflammatory signalling, extracellular matrix remodelling, and endocrine activation that collectively promote premature labour. We further integrate underexplored mechanistic pathways, including mitochondrial dynamics and mitophagy, ferroptosis, nicotinamide adenine dinucleotide (NAD⁺) metabolism, inflammasome activation, extracellular vesicle signalling, and deoxyribonucleic acid (DNA) damage responses. These interconnected pathways interact through damage-associated molecular patterns (DAMPs), cytokines, and extracellular vesicles to coordinate pathological crosstalk across the maternal-fetal interface. Emerging multi-marker biomarker strategies and targeted therapeutic approaches, including mitochondrial antioxidants, senolytic agents, and inflammasome inhibitors, are also discussed within this framework. Mitochondrial dysfunction and cellular senescence represent central biological axes linking molecular stress with premature activation of labour pathways in sPTB. Conceptualizing sPTB as accelerated gestational aging provides a unifying framework for integrating diverse mechanistic pathways, refining risk stratification, and guiding the development of targeted, precision-based interventions to reduce the global burden of prematurity.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-026-02394-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taginostat, a new quinolone-based HDAC6 inhibitor, promotes apoptosis of chronic lymphocytic leukemia cells in vitro and in vivo by activating STAT4","authors":"Vanessa Tatangelo,&nbsp;Gabriele Carullo,&nbsp;Ludovica Lopresti,&nbsp;Cristina Ulivieri,&nbsp;Simone Brogi,&nbsp;Stefania Butini,&nbsp;Matteo Gatta,&nbsp;Nagaja Capitani,&nbsp;Federica Rungo,&nbsp;Maria Carmela Cavallo,&nbsp;Alessandro Gozzetti,&nbsp;Monica Bocchia,&nbsp;Monica Tozzi,&nbsp;Sara Ciofini,&nbsp;Sandra Gemma,&nbsp;Cosima T Baldari,&nbsp;Giuseppe Campiani,&nbsp;Laura Patrussi","doi":"10.1007/s10495-026-02393-0","DOIUrl":"10.1007/s10495-026-02393-0","url":null,"abstract":"<div><p>Chronic lymphocytic leukemia (CLL) is a hematological malignancy characterized by the accumulation of mature CD5⁺ B cells largely due to defective apoptosis. Prolonged leukemic cell survival has been linked to downregulation of the pro-apoptotic adaptor p66Shc and its transcription factor STAT4, both of which are typically reduced in CLL patients. To date, a clear mechanistic explanation for STAT4 deficiency in CLL has not yet been provided. Restoring STAT4 expression or activating its residual function may represent an attractive therapeutic strategy. Histone deacetylase 6 (HDAC6) directly deacetylates and suppresses STAT4 in T lymphocytes, suggesting that a similar mechanism may operate in CLL cells. In this study, we hypothesized that HDAC6-mediated STAT4 inhibition also occurs in CLL cells and contributes to leukemic cell survival. Accordingly, we tested the potent HDAC6 inhibitor Taginostat (HDAC6 IC₅₀ = 7.9 nM) and found that it enhanced p66Shc expression and restored apoptosis in CLL cells. These effects were reproduced by HDAC6 silencing. Flow cytometric and western blot analyses showed that Taginostat boosted residual STAT4 activity by enhancing its phosphorylation. Moreover, transient transfection with STAT4-luciferase or STAT4-green fluorescent protein (GFP) constructs demonstrated that Taginostat promoted both the nuclear translocation and transcriptional activity of STAT4. In addition, in vivo experiments conducted in the Eµ-TCL1 mouse model of CLL demonstrated that Taginostat treatment counteracted disease development, significantly reducing the leukemia burden. Collectively, these findings validate HDAC6 inhibition as a valuable therapeutic strategy for promoting STAT4 activation in CLL cells, restoring the apoptotic cascade, and counteracting disease progression.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148380317","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":"Correction: Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers","authors":"Nilufer Ercin,&nbsp;Nail Besli,&nbsp;Merve Beker,&nbsp;Ulkan Celik","doi":"10.1007/s10495-026-02387-y","DOIUrl":"10.1007/s10495-026-02387-y","url":null,"abstract":"","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-026-02387-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148380318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis","authors":"Ai-Qian Liu,&nbsp;Jongwon Byun,&nbsp;Nan Nan Yu,&nbsp;Mei-Hua Jin,&nbsp;Ying-Hao Han,&nbsp;Dong Seok Lee,&nbsp;Dong-Hun Lee,&nbsp;Hu-Nan Sun","doi":"10.1007/s10495-026-02384-1","DOIUrl":"10.1007/s10495-026-02384-1","url":null,"abstract":"<div><p>Tissue fibrosis represents the common terminal pathological features of multiple chronic diseases, yet effective therapeutic agents capable of retarding fibrotic progression remain limited. This review systematically delineates the antifibrotic pharmacological profile of salidroside and elucidates its multi-target synergistic mechanisms across renal, hepatic, pulmonary, and cardiac fibrosis. Our comprehensive analysis reveals that salidroside exerts multifaceted antifibrotic effects through the integrated modulation of diverse signaling networks. Specifically, it concurrently suppresses pro-fibrotic pathways including TGF-β1/Smad, Wnt/β-catenin, and PI3K/Akt/mTOR to attenuate extracellular matrix deposition and myofibroblast activation; activates the Nrf2-Keap1 antioxidant axis and the AMPK/SIRT1/PGC-1α energy metabolism pathway to enhance mitochondrial biogenesis and scavenge reactive oxygen species; and blocks p38/JNK and NF-κB inflammatory cascades to reduce TNF-α, IL-6, and IL-1β secretion. Notably, SIRT1 serves as a central hub mediating the crosstalk between ferroptosis and autophagy via the SIRT1/PINK1 axis, while simultaneously coordinating antioxidant-anti-inflammatory amplification and bidirectional inhibition of fibrotic signaling, thereby forming positive-feedback loops that circumvent compensatory pathway activation inherent to single-target interventions. Furthermore, salidroside indirectly ameliorates fibrotic microenvironments through gut microbiota remodeling and modulation of gut-organ axis metabolites including LPS and TMAO. Despite these promising preclinical findings, the clinical translation of salidroside is constrained by poor oral bioavailability, limited organ-targeting specificity, and a paucity of large-scale clinical evidence. Collectively, these findings establish salidroside as a promising multi-target antifibrotic candidate and provide a comprehensive mechanistic framework for its development into a cross-organ precision therapeutic, while highlighting the urgent need for optimized delivery systems and rigorous clinical validation to bridge the gap between basic research and clinical application.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366705","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}