Cell Death Discovery最新文献

Inhibition of anti-apoptotic Bcl-2 family members promotes synergistic cell death with ER stress inducers by disrupting autophagy in glioblastoma. 抑制抗凋亡Bcl-2家族成员通过破坏胶质母细胞瘤的自噬促进与内质网应激诱导剂的协同细胞死亡。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-24 DOI: 10.1038/s41420-025-02632-4

Tianyi Huang, Satoshi Takagi, Sumie Koike, Ryohei Katayama

{"title":"Inhibition of anti-apoptotic Bcl-2 family members promotes synergistic cell death with ER stress inducers by disrupting autophagy in glioblastoma.","authors":"Tianyi Huang, Satoshi Takagi, Sumie Koike, Ryohei Katayama","doi":"10.1038/s41420-025-02632-4","DOIUrl":"https://doi.org/10.1038/s41420-025-02632-4","url":null,"abstract":"Glioblastoma (GBM) remains one of the most aggressive and challenging brain tumors. Unfortunately, current clinical treatment options offer limited efficacy, highlighting the necessity for uncovering novel therapeutic strategies. Here, monotherapy and combination library screening were employed, and identified that the efficacy of obatoclax, a pan-Bcl-2 family inhibitor, was improved significantly when combined with ER-stress inducers, including tunicamycin. Combinatorial knockdown of anti-apoptotic proteins confirmed that the loss of Mcl-1 and Bcl-xL synergistically enhanced apoptosis under ER stress conditions. Although ER stress inducers triggered the stress response in GBM cells, obatoclax co-treatment enhanced this response by upregulating ATF-4 and CHOP, which promoted apoptosis along with increased caspase 3/7 activity and cleavage of PARP. ATF-4 knockdown significantly decreased the apoptosis induced by obatoclax and tunicamycin co-treatment and reduced the expression of CHOP and BIM. Under ER stress responses, GBM cells exerted an autophagy response to recover from the stress condition; however, obatoclax co-treatment disrupted the autophagy responses, particularly by disrupting autophagic cargo degradation. Our findings suggest that targeting Mcl-1 and Bcl-xL, coupled with ER-stress induction, could be a promising strategy for the treatment of GBM, highlighting the potential for combination therapies involving pan-Bcl-2 family inhibitors to overcome current limitations in the treatment of GBM.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"340"},"PeriodicalIF":6.1,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706343","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}

引用次数: 0

Strawberry notch 1 safeguards neuronal genome via regulation of Yeats4 expression. 草莓notch 1通过调控yeat4的表达来保护神经元基因组。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-24 DOI: 10.1038/s41420-025-02640-4

Dai Ihara, Ayano Narumoto, Yukie Kande, Tomoki Hayashi, Yasuaki Ikuno, Manabu Shirai, Masaki Wakabayashi, Ryo Nitta, Hayato Naka-Kaneda, Yu Katsuyama

{"title":"Strawberry notch 1 safeguards neuronal genome via regulation of Yeats4 expression.","authors":"Dai Ihara, Ayano Narumoto, Yukie Kande, Tomoki Hayashi, Yasuaki Ikuno, Manabu Shirai, Masaki Wakabayashi, Ryo Nitta, Hayato Naka-Kaneda, Yu Katsuyama","doi":"10.1038/s41420-025-02640-4","DOIUrl":"https://doi.org/10.1038/s41420-025-02640-4","url":null,"abstract":"Neurons are subjected to various stresses, including high metabolic demand, physiological activity, and transcriptional regulation, to which their genomic DNA are vulnerable. Genome stability of neurons is essential for proper physiological brain function. Failure in accurate genomic DNA repair can result in abnormal neuronal functions or cell death. Genomic instability has been implicated in increased risks of neurodevelopmental and neurodegenerative disorders. However, the molecular mechanisms underlying neuronal genome stability remain poorly understood. Mutations in the Strawberry Notch Homolog 1 (SBNO1) have been suggested to contribute to these disorders. Here, we investigated the molecular mechanisms underlying histological abnormalities observed in the cortex of Sbno1 knockout (KO) mice. Comprehensive gene expression analysis revealed that Sbno1 KO affects the expression of genes related to cell survival, consistent with the increased apoptosis observed in Sbno1 KO cortices. Among the genes downregulated in Sbno1 KO, we focused on Yeats4. Overexpression of Yeats4 rescued the accumulation of genomic DNA damage and cell death caused by Sbno1 deletion. These findings suggest that Sbno1 is critical in safeguarding the neuronal genome, at least in part, via regulating Yeats4 expression.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"342"},"PeriodicalIF":6.1,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706344","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}

引用次数: 0

The Hippo signaling pathway modulates pancreatic tissue homeostasis. Hippo信号通路调节胰腺组织稳态。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-24 DOI: 10.1038/s41420-025-02636-0

Xiaoyan Wang, Jiajing Du, Haiyun Li, Zhiwei Cao, Zhonghua Cheng, Zuoyun Wang

引用次数: 0

Cancer-associated fibroblasts in cancer drug resistance and cancer progression: a review. 癌症相关成纤维细胞在癌症耐药和癌症进展中的研究进展

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-24 DOI: 10.1038/s41420-025-02566-x

Hideyuki Masuda

引用次数: 0

The RNF8/OPTN/KDM6A axis controls macrophage polarization to maintain testicular microenvironment homeostasis. RNF8/OPTN/KDM6A轴控制巨噬细胞极化维持睾丸微环境稳态。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-24 DOI: 10.1038/s41420-025-02641-3

Yanan Guo, Peng Xia, Yixiao Tian, Daosen Fu, Xiaohui Hu, Kun Xie, Wenhao Dong, Wei Zhang, Disheng Liu, Rong Shen, Degui Wang

{"title":"The RNF8/OPTN/KDM6A axis controls macrophage polarization to maintain testicular microenvironment homeostasis.","authors":"Yanan Guo, Peng Xia, Yixiao Tian, Daosen Fu, Xiaohui Hu, Kun Xie, Wenhao Dong, Wei Zhang, Disheng Liu, Rong Shen, Degui Wang","doi":"10.1038/s41420-025-02641-3","DOIUrl":"https://doi.org/10.1038/s41420-025-02641-3","url":null,"abstract":"Dysregulated immune responses may erroneously target normal reproductive tissues, thereby compromising the proper functioning of the reproductive system. Macrophages are the most abundant immune cells in the testes, however, the role of macrophages in spermatogenic function is not yet clear. This study indicated that the increase of pro-inflammatory macrophages impaired the development of spermatogenic cells, and the deficiency of RNF8 led to a proinflammatory state in the testicular microenvironment and diminished sperm production in mice. RNF8 mainly assembled K63-branched ubiquitin chains on autophagy receptor OPTN at K448 thus causing OPTN activation. The increased ubiquitination of OPTN promoted degradation of KDM6A via the autophagy-lysosome pathway, thereby inhibiting macrophage polarization towards the pro-inflammatory type and maintaining an immune privilege state in the testicular microenvironment. This homeostasis could be collapsed once the RNF8-OPTN-KDM6A axis was abnormal, subsequently resulting in remodeling of the testicular microenvironment. This study reveals the underlying mechanism of RNF8 on male reproduction, and the pro-inflammatory microenvironment resulting from RNF8 deficiency hindered spermatogenic cell differentiation, thereby impairing spermatogenic function.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"339"},"PeriodicalIF":6.1,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706445","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}

引用次数: 0

RBM17 promotes hepatocellular carcinoma progression by regulating lipid metabolism and immune microenvironment: implications for therapeutic targeting. RBM17通过调节脂质代谢和免疫微环境促进肝细胞癌进展：对治疗靶向的影响

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-23 DOI: 10.1038/s41420-025-02642-2

Zengbin Wang, Jiayu Liu, Yiting Lai, Qing Zhong, Qian Su, Linqing Wu, Zhihong Wang, Zhuting Fang

{"title":"RBM17 promotes hepatocellular carcinoma progression by regulating lipid metabolism and immune microenvironment: implications for therapeutic targeting.","authors":"Zengbin Wang, Jiayu Liu, Yiting Lai, Qing Zhong, Qian Su, Linqing Wu, Zhihong Wang, Zhuting Fang","doi":"10.1038/s41420-025-02642-2","DOIUrl":"https://doi.org/10.1038/s41420-025-02642-2","url":null,"abstract":"Variable splicing (AS) plays important roles in tumor progression. However, the role of the AS factor RBM17 in the progression of hepatocellular carcinoma (HCC) has not yet been elucidated. We used label-free proteomics, single-cell sequencing (scRNA-seq), high throughput sequencing, flow cytometry (FCM), liquid Chromatography-tandem mass spectrometry (LC‒MS/MS), multiparametric immunofluorescence (mIF) and chromatin immunoprecipitation (Chip), to explore the relationship between RBM17 regulation of HCC cell lipid metabolism and the immune microenvironment. Our findings revealed that RBM17 is significantly overexpressed in HCC tissue and is positively correlated with poor prognosis. We found a positive correlation between RBM17 expression and M2 macrophage infiltration. Mechanistically, RBM17 promotes M2 macrophage infiltration by inducing taurocholic acid (T-CA) production, which is achieved through enhancing exon exclusion of CSAD precursor mRNA. Additionally, RBM17 modulates fatty acid metabolism and CD8+ T cell infiltration by regulating exon skipping in HACD3 precursor mRNA. Furthermore, RUNX1 activates RBM17 expression and regulates downstream CSAD/T-CA and HACD3/FFA signaling. Importantly, targeting RBM17 can prevent HCC progression, suggesting its potential as a therapeutic target for HCC. Our findings provide new insights into the mechanisms underlying immune cell infiltration and metabolism in HCC and identify RBM17 as a promising therapeutic target.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"338"},"PeriodicalIF":6.1,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697743","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}

引用次数: 0

MARCO expression on myeloid-derived suppressor cells is essential for their differentiation and immunosuppression. 髓源性抑制细胞的MARCO表达对其分化和免疫抑制至关重要。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-22 DOI: 10.1038/s41420-025-02627-1

Sijia Liu, Binle Tian, Na Wang, Zhilong Wang, Wen Zhang, Qi Li, JianFei Wang, Guo-Huang Fan, Caicun Zhou

{"title":"MARCO expression on myeloid-derived suppressor cells is essential for their differentiation and immunosuppression.","authors":"Sijia Liu, Binle Tian, Na Wang, Zhilong Wang, Wen Zhang, Qi Li, JianFei Wang, Guo-Huang Fan, Caicun Zhou","doi":"10.1038/s41420-025-02627-1","DOIUrl":"https://doi.org/10.1038/s41420-025-02627-1","url":null,"abstract":"Myeloid-derived suppressor cells (MDSCs) significantly contribute to the immunosuppressive tumor microenvironment (TME), and targeted inhibition of MDSCs is a potential therapeutic strategy against cancer. Here, we identify macrophage receptor with collagenous structure (MARCO) as a critical regulator of MDSC differentiation and immunosuppression in breast cancer. The present study demonstrates that MARCO is expressed on MDSCs, and breast tumor-derived exosomes (TDEs) enriched with macrophage migration inhibitory factor (MIF) promote MDSC differentiation and amplify immunosuppressive activity by up-regulating MARCO. Genetic ablation of MARCO in a murine breast cancer model attenuated tumor growth, accompanied by reduced monocytic MDSCs (M-MDSCs) and total tumor-associated macrophages (TAMs), along with enhanced infiltration of CD8+ T cells and natural killer (NK) cells. Furthermore, we developed a specific MARCO down-regulation-promoting monoclonal antibody that impeded TDE-induced MDSC differentiation and immunosuppression. In vivo, MARCO down-regulating antibody suppressed tumor growth and reprogrammed the TME by diminishing immunosuppressive MDSCs and TAMs and revitalizing CD8+ T cells and NK cells. Strikingly, combining the MARCO down-regulating antibody with PD-1 blockade synergistically enhanced anti-tumor efficacy. This work establishes MARCO as a key regulator of MDSC-mediated immunosuppression and presents a compelling case for the inclusion of MARCO as a therapeutic target in cancer immunotherapy.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"337"},"PeriodicalIF":6.1,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689034","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}

引用次数: 0

Epithelial-mesenchymal transition in colorectal cancer metastasis and progression: molecular mechanisms and therapeutic strategies. 结直肠癌转移和进展中的上皮-间质转化：分子机制和治疗策略。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-22 DOI: 10.1038/s41420-025-02593-8

Fangfang Nie, Xue Sun, Jizhuo Sun, Jingdong Zhang, Yuanhe Wang

{"title":"Epithelial-mesenchymal transition in colorectal cancer metastasis and progression: molecular mechanisms and therapeutic strategies.","authors":"Fangfang Nie, Xue Sun, Jizhuo Sun, Jingdong Zhang, Yuanhe Wang","doi":"10.1038/s41420-025-02593-8","DOIUrl":"https://doi.org/10.1038/s41420-025-02593-8","url":null,"abstract":"Colorectal cancer (CRC) continues to be a major contributor to cancer-associated death, with metastatic disease posing substantial therapeutic challenges. The epithelial-mesenchymal transition (EMT) orchestrates the transformation of polarized epithelial cells into motile mesenchymal phenotypes, characterized by enhanced migratory capacity and invasive properties. EMT is central to CRC metastasis and progression, particularly concerning its contribution to invasion, internal infiltration, and colonization. Beyond metastasis, EMT facilitates cancer cells' adaptation to diverse microenvironments, gain of stem cell-like characteristics, metabolic reprogramming, and evasion of therapeutic interventions. EMT signatures are emerging as potential prognostic biomarkers, offering valuable insights for real-time disease surveillance and personalized therapeutic strategies. Targeting EMT presents a promising therapeutic avenue to improve drug sensitivity and counteract resistance in CRC. This review systematically examines the molecular mechanisms regulating EMT in CRC, including key transcription factors; post-translational and epigenetic modifications; non-coding RNAs; and pivotal signaling pathways. Additionally, we evaluate the clinical implications of EMT in CRC progression and metastasis and critically assess emerging therapeutic strategies targeting EMT. This study lays the groundwork for developing more efficient interventions to mitigate metastasis and enhance treatment outcomes and patient survival by elucidating the intricate molecular networks that govern EMT and its contributions to CRC pathology.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"336"},"PeriodicalIF":6.1,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689033","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}

引用次数: 0

EIF3B stabilizes MAP2K2 to activate the ERK pathway and promote the progression of laryngeal squamous cell carcinoma. EIF3B稳定MAP2K2，激活ERK通路，促进喉鳞癌的进展。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-21 DOI: 10.1038/s41420-025-02634-2

Jie Tan, Xueshi Li, Yuguang Wang, Lin Wang, Xingguo Zhao, Yixu Wang, Meng Cui

{"title":"EIF3B stabilizes MAP2K2 to activate the ERK pathway and promote the progression of laryngeal squamous cell carcinoma.","authors":"Jie Tan, Xueshi Li, Yuguang Wang, Lin Wang, Xingguo Zhao, Yixu Wang, Meng Cui","doi":"10.1038/s41420-025-02634-2","DOIUrl":"10.1038/s41420-025-02634-2","url":null,"abstract":"To elucidate the role of eukaryotic translation initiation factor 3 subunit B (EIF3B) in laryngeal squamous cell carcinoma (LSCC) progression and its regulatory mechanism. Integrated bioinformatics analysis (GEO, TCGA), immunohistochemistry (IHC), lentiviral-mediated gene knockdown/overexpression, co-immunoprecipitation (Co-IP), Western blotting (WB), and in vivo xenograft models were employed. Clinically, our findings revealed an upregulation of EIF3B expression in LSCC, with its abnormally high levels significantly correlating with poor survival outcomes among patients. Functionally, ablation of EIF3B potently inhibited cancer cell proliferation, colony formation, and migratory abilities. Mechanistically, EIF3B stabilized MAP2K2 via direct interaction with its P3 domain, inhibiting VHL-mediated ubiquitination at K169. Notably, MAP2K2 kinase activity was essential for EIF3B-driven ERK phosphorylation and downstream oncogenic signaling. Moreover, EIF3B overexpression accelerated tumor growth in xenograft models, which was rescued by MAP2K2 knockdown. In Conclusion, EIF3B promotes LSCC progression by stabilizing MAP2K2, activating the ERK/MAPK pathway, and disrupting VHL-mediated proteostasis. Targeting the EIF3B-MAP2K2 axis may offer therapeutic strategies for LSCC.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"333"},"PeriodicalIF":6.1,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12280010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682041","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}

引用次数: 0

Emerging regulated cell death mechanisms in bone remodeling: decoding ferroptosis, cuproptosis, disulfidptosis, and PANoptosis as therapeutic targets for skeletal disorders. 骨重塑中新出现的受调节细胞死亡机制：解读作为骨骼疾病治疗靶点的铁下垂、铜下垂、二硫下垂和PANoptosis。

IF 6.1 2区生物学

Cell Death Discovery Pub Date : 2025-07-21 DOI: 10.1038/s41420-025-02633-3

Hai-Ting Hu, Zhen-Yu Zhang, Zi -Xin Luo, Hui-Bo Ti, Jun-Jie Wu, Hao Nie, Zheng-Dong Yuan, Xian Wu, Ke-Yue Zhang, Shu-Wen Shi, Yi-Qing Qian, Xin-Chen Wang, Jing-Jing Wu, Xia Li, Feng-Lai Yuan

{"title":"Emerging regulated cell death mechanisms in bone remodeling: decoding ferroptosis, cuproptosis, disulfidptosis, and PANoptosis as therapeutic targets for skeletal disorders.","authors":"Hai-Ting Hu, Zhen-Yu Zhang, Zi -Xin Luo, Hui-Bo Ti, Jun-Jie Wu, Hao Nie, Zheng-Dong Yuan, Xian Wu, Ke-Yue Zhang, Shu-Wen Shi, Yi-Qing Qian, Xin-Chen Wang, Jing-Jing Wu, Xia Li, Feng-Lai Yuan","doi":"10.1038/s41420-025-02633-3","DOIUrl":"10.1038/s41420-025-02633-3","url":null,"abstract":"The adult skeleton preserves its structural and functional integrity through continuous bone remodeling, a process tightly regulated by osteoblasts, osteoclasts, and osteocytes. Disruptions to this balance contribute to skeletal pathologies like osteoporosis and periodontitis, underscoring the need to understand the mechanisms governing bone homeostasis. Regulated cell death (RCD) plays a key role in bone remodeling by modulating the activity of osteoblasts and osteoclasts. Recent advances have revealed novel RCD modalities: ferroptosis, cuproptosis, disulfidptosis, and PANoptosis, each with unique molecular mechanisms and pathophysiological implications in bone disorders. So we want to elucidate the molecular mechanisms, signaling cascades, and roles of these four novel RCD modalities in bone remodeling and skeletal homeostasis. We explore their potential involvement in bone-related pathologies, emphasizing the crucial roles of osteoblasts, osteoclasts, and osteocytes in maintaining skeletal integrity. By synthesizing emerging evidence, we aim to identify therapeutic targets and propose innovative strategies for managing skeletal disorders, advancing research in bone health and providing novel insights for clinical translation. Emerging regulated cell death mechanisms in bone remodeling.","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"335"},"PeriodicalIF":6.1,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12280121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682042","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}

引用次数: 0