Cell Death Discovery最新文献

{"title":"TBK1 is involved in programmed cell death and ALS-related pathways in novel zebrafish models.","authors":"Quentin Raas, Gregoire Haouy, Hortense de Calbiac, Elena Pasho, Anca Marian, Ida Chiara Guerrera, Marion Rosello, Patrick Oeckl, Filippo Del Bene, Alberto Catanese, Sorana Ciura, Edor Kabashi","doi":"10.1038/s41420-025-02374-3","DOIUrl":"10.1038/s41420-025-02374-3","url":null,"abstract":"<p><p>Pathogenic mutations within the TBK1 gene leading to haploinsufficiency are causative of amyotrophic lateral sclerosis (ALS). This gene is linked to autophagy and inflammation, two cellular mechanisms reported to be dysregulated in ALS patients, although its functional role in the pathogenesis could involve other players. We targeted the TBK1 ortholog in zebrafish, an optimal vertebrate model for investigating genetic defects in neurological disorders. We generated zebrafish models with invalidating tbk1 mutations using CRISPR-Cas9 or tbk1 knockdown models using antisense morpholino oligonucleotide (AMO). The early motor phenotype of zebrafish injected with tbk1 AMO beginning at 2 days post fertilization (dpf) is associated with the degeneration of motor neurons. In parallel, CRISPR-induced tbk1 mutants exhibit impaired motor function beginning at 5 dpf and increased lethality beginning at 9 dpf. A metabolomic analysis showed an association between tbk1 loss and severe dysregulation of nicotinamide metabolism, and incubation with nicotinamide riboside rescued the motor behavior of tbk1 mutant zebrafish. Furthermore, a proteomic analysis revealed increased levels of inflammatory markers and dysregulation of programmed cell death pathways. Necroptosis appeared to be strongly activated in TBK1 fish, and larvae treated with the necroptosis inhibitor necrosulfonamide exhibited improved survival. Finally, a combined analysis of mutant zebrafish and TBK1-mutant human motor neurons revealed dysregulation of the KEGG pathway \"ALS\", with disrupted nuclear-cytoplasmic transport and increased expression of STAT1. These findings point toward a major role for necroptosis in the degenerative features and premature lethality observed in tbk1 mutant zebrafish. Overall, the novel tbk1-deficient zebrafish models offer a great opportunity to better understand the cascade of events leading from the loss of tbk1 expression to the onset of motor deficits, with involvement of a metabolic defect and increased cell death, and for the development of novel therapeutic avenues for ALS and related neuromuscular diseases.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"98"},"PeriodicalIF":6.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613694","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":"Ex.50.T aptamer impairs tumor-stroma cross-talk in breast cancer by targeting gremlin-1.","authors":"Cristina Quintavalle, Francesco Ingenito, Giuseppina Roscigno, Birlipta Pattanayak, Carla Lucia Esposito, Alessandra Affinito, Danilo Fiore, Gianluca Petrillo, Silvia Nuzzo, Bartolomeo Della Ventura, Federica D'Aria, Concetta Giancola, Stefania Mitola, Elisabetta Grillo, Marinella Pirozzi, Greta Donati, Francesco Saverio Di Leva, Luciana Marinelli, Zoran Minic, Francesca De Micco, Guglielmo Thomas, Maxim V Berezovski, Gerolama Condorelli","doi":"10.1038/s41420-025-02363-6","DOIUrl":"10.1038/s41420-025-02363-6","url":null,"abstract":"<p><p>The tumor microenvironment profoundly influences tumor complexity, particularly in breast cancer, where cancer-associated fibroblasts play pivotal roles in tumor progression and therapy resistance. Extracellular vesicles are involved in mediating communication within the TME, specifically highlighting their role in promoting the transformation of normal fibroblasts into cancer-associated fibroblasts. Recently, we identified an RNA aptamer, namely ex.50.T, that binds with remarkable affinity to extracellular vesicles shed from triple-negative breast cancer cells. Here, through in vitro assays and computational analyses, we demonstrate that the binding of ex.50.T to extracellular vesicles and parental breast cancer cells is mediated by recognition of gremlin-1 (GREM1), a bone morphogenic protein antagonist implicated in breast cancer aggressiveness and metastasis. Functionally, we uncover the role of ex.50.T as an innovative therapeutic agent in the process of tumor microenvironment re-modeling, impeding GREM1 signaling, blocking triple-negative breast cancer extracellular vesicles internalization in recipient cells, and counteracting the transformation of normal fibroblasts into cancer-associated fibroblasts. Altogether, our findings highlight ex.50.T as a novel therapeutical avenue for breast cancer and potentially other GREM1-dependent malignancies, offering insights into disrupting TME dynamics and enhancing cancer treatment strategies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"94"},"PeriodicalIF":6.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603844","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":"Correction: A Y178C rhodopsin mutation causes aggregation and comparatively severe retinal degeneration.","authors":"Sreelakshmi Vasudevan, Paul S-H Park","doi":"10.1038/s41420-025-02346-7","DOIUrl":"10.1038/s41420-025-02346-7","url":null,"abstract":"","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"95"},"PeriodicalIF":6.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603927","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":"Cell death in tumor microenvironment: an insight for exploiting novel therapeutic approaches.","authors":"Wenxin Wang, Tong Li, Kui Wu","doi":"10.1038/s41420-025-02376-1","DOIUrl":"10.1038/s41420-025-02376-1","url":null,"abstract":"<p><p>Cell death is critical in tumor biology. The common cancer therapies can cause cell death and alleviate tumor, while the cancer cells can develop a resistance to cell death and survive from the therapies. Thus, not only observing the alternative mechanisms of tumor cells resistant to cell death, but also understanding the intricate dynamics of cell death processes within the tumor microenvironment (TME), are essential for tailoring effective therapeutic strategies. High-throughput sequencing technologies have revolutionized cancer research by enabling comprehensive molecular profiling. Recent advances in single cell sequencing have unraveled the heterogeneity of TME components, shedding light on their complex interactions. In this review, we explored the interplay between cell death signaling and the TME, summarised the potential drugs inducing cell death in pre-clinical stage, reviewed some studies applying next-generation sequencing technologies in cancer death research, and discussed the future utilization of updated sequencing platforms in screening novel treatment methods targeted cell death. In conclusion, leveraging multi-omics technologies to dissect cell death signaling in the context of the TME holds great promise for advancing cancer research and therapy development.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"93"},"PeriodicalIF":6.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596332","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":"Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism.","authors":"Chun-Cheng Yang, Yu-Chuan Yan, Guo-Qiang Pan, Guang-Xiao Meng, Xiao Zhang, Lun-Jie Yan, Zi-Niu Ding, Dong-Xu Wang, Rui-Zhe Li, Guang-Zhen Li, Zhao-Ru Dong, Tao Li","doi":"10.1038/s41420-025-02378-z","DOIUrl":"10.1038/s41420-025-02378-z","url":null,"abstract":"<p><p>Thyroid hormones (THs) dysfunctions have been demonstrated to be associated with the risk of developing different types of cancers. The role of THs in regulating hepatocellular carcinoma (HCC) progression is still controversial. We demonstrated that T3 can inhibit HCC progression by enhancing the expression of THRSP. Mechanistically, T3 can activate tumor suppressor LKB1/AMPK/Raptor signaling as well as oncogenic PI3K/Akt signaling in HCC. Interestingly, T3-induced THRSP can augment the activation of LKB1/AMPK/Raptor signaling, yet inhibit T3-induced PI3K/Akt signaling activation, thereby preventing mTOR-induced nuclear translocation of HIF-1α, and ultimately suppressing ENO2-induced glycolysis and HCC progression. More importantly, the exogenous T3 enhances the antitumor effect of multikinase inhibitor lenvatinib in vitro and in vivo by regulating glycolysis. Our findings reveal the role and mechanism of THs in HCC progression and glucose metabolism and provide new potential therapeutic strategies for HCC treatment and drug resistance reversal.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"92"},"PeriodicalIF":6.1,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584822","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":"Mitochondrial priming and response to BH3 mimetics in \"one-two punch\" senogenic-senolytic strategies.","authors":"Júlia López, Àngela Llop-Hernández, Sara Verdura, Eila Serrano-Hervás, Eva Martinez-Balibrea, Joaquim Bosch-Barrera, Eduard Teixidor, Eugeni López-Bonet, Begoña Martin-Castillo, Josep Sardanyés, Tomás Alarcón, Ruth Lupu, Elisabet Cuyàs, Javier A Menendez","doi":"10.1038/s41420-025-02379-y","DOIUrl":"10.1038/s41420-025-02379-y","url":null,"abstract":"<p><p>A one-two punch sequential regimen of senescence-inducing agents followed by senolytic drugs has emerged as a novel therapeutic strategy in cancer. Unfortunately, cancer cells undergoing therapy-induced senescence (TIS) vary widely in their sensitivity to senotherapeutics, and companion diagnostics to predict the response of TIS cancer cells to a specific senolytic drug are lacking. Here, we hypothesized that the ability of the BH3 profiling assay to functionally measure the mitochondrial priming state-the proximity to the apoptotic threshold-and the dependencies on pro-survival BCL-2 family proteins can be exploited to inform the sensitivity of TIS cancer cells to BH3-mimetics. Replicative, mitotic, oxidative, and genotoxic forms of TIS were induced in p16-null/p53-proficient, BAX-deficient, and BRCA1-mutant cancer cells using mechanistically distinct TIS-inducing cancer therapeutics, including palbociclib, alisertib, doxorubicin, bleomycin, and olaparib. When the overall state of mitochondrial priming and competence was determined using activator peptides, the expected increase in overall mitochondrial priming was an exception rather than a generalizable feature across TIS phenotypes. A higher level of overall priming paralleled a higher sensitivity of competent TIS cancer cells to BCL-2/BCL-xL- and BCL-xL-targeted inhibitors when comparing TIS phenotypes among themselves. Unexpectedly, however, TIS cancer cells remained equally or even less overally primed than their proliferative counterparts. When sensitizing peptides were used to map dependencies on anti-apoptotic BCL-2 family proteins, competent TIS cancer cells appeared to share a dependency on BCL-xL. Furthermore, regardless of senescence-inducing therapeutic, stable/transient senescence acquisition, or genetic context, all TIS phenotypes shared a variable but significant senolytic response to the BCL-xL-selective BH3 mimetic A1331852. These findings may help to rethink the traditional assumption of the primed apoptotic landscape of TIS cancer cells. BCL-xL is a conserved anti-apoptotic effector of the TIS BCL2/BH3 interactome that can be exploited to maximize the efficacy of \"one-two punch\" senogenic-senolytic strategies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"91"},"PeriodicalIF":6.1,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584821","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":"CXCL16 knockout inhibit asthma airway inflammation by suppressing H2-DM molecular mediated antigen presentation.","authors":"Ting-Ting Liu, Zhi Zhang, Jing Deng, Chang-Yu Shi, Shuai Zheng, Li-Xin Jia, Jie Du, Chunmei Piao","doi":"10.1038/s41420-025-02371-6","DOIUrl":"10.1038/s41420-025-02371-6","url":null,"abstract":"<p><p>The inflammatory microenvironment influences dendritic cell-mediated antigen presentation to regulate asthma Th2 inflammation. The scavenger receptor is expressed on DCs and regulates antigen presentation and T priming. However, whether the transmembrane scavenger receptor (SR-PSOX/CXCL16) regulates the phenotype and antigen presentation function of DCs remains unclear. We found that CXCL16 is mainly expressed on DCs in the lung tissues of asthma patients and asthma mice. CXCL16 knockout led to the suppression of airway inflammation, mucus overproduction, and airway hyperresponsiveness in Aspergillus-induced asthma. In addition, the adoptive transfer of Aspergillus-pulsed DCs shows the CXCL16⁺ DCs exerted a promoting role in airway inflammation, the CXCL16^- DCs inhibit airway inflammation. Additionally, RNA sequencing and flow cytometry data revealed that CXCL16 knockout inhibits airway inflammation by suppressing the antigen processing and presentation function of DCs, which was mediated by MHC II chaperone H2-DM. Furthermore, we found CXCL16 knockout suppressed dendritic cells differentiated forward to cDC2b subtype which is mainly charged with antigen presentation to T cell. In conclusion, we found that CXCL16 downregulated the capacity of DC antigen processing and presentation to suppress airway inflammation by reducing H2-DM expression which mediated DC differentiation. The study suggested that inhibition of CXCL16 can be a potential therapy for asthma.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"90"},"PeriodicalIF":6.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572202","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":"Endothelial senescence induced by PAI-1 promotes endometrial fibrosis.","authors":"Jing Wu, Jie Wang, Zhongrui Pei, Yaru Zhu, Xier Zhang, Zihan Zhou, Chunying Ye, Minmin Song, Yali Hu, Pingping Xue, Guangfeng Zhao","doi":"10.1038/s41420-025-02377-0","DOIUrl":"10.1038/s41420-025-02377-0","url":null,"abstract":"<p><p>Intrauterine adhesions (IUAs), also known as Asherman's syndrome (AS), represent a significant cause of uterine infertility for which effective treatment remains elusive. The endometrium's ability to regenerate cyclically depends heavily on the growth and regression of its blood vessels. However, trauma to the endometrial basal layer can disrupt the subepithelial capillary plexus, impeding regeneration. This damage results in the replacement of native cells with fibroblasts and myofibroblasts, ultimately leading to fibrosis. Endothelial cells (ECs) play a pivotal role in the vascular system, extending beyond their traditional barrier function. Through single-cell sequencing and experimental validation, we discovered that ECs undergo senescence in IUA patients, impairing angiogenesis and fostering stromal cell fibrosis. Further analysis revealed significant interactions between ECs and PAI-1+ stromal cells. PAI-1, derived from stromal cells, promotes EC senescence via the urokinase-type plasminogen activator receptor (uPAR). Notably, prior to fibrosis onset, TGF-β upregulates PAI-1 expression in stromal cells in a SMAD dependent manner. In an IUA mouse model, inhibiting PAI-1 mitigated EC senescence and endometrial fibrosis. Our findings underscore the crucial role of EC senescence in IUA pathogenesis, contributing to vascular reduction and fibrosis. Targeting PAI-1 represents a promising therapeutic strategy to suppress EC senescence and alleviate endometrial fibrosis, offering new insights into the treatment of IUAs.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"89"},"PeriodicalIF":6.1,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572237","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 Caveolin-1 for enhanced rotator cuff repair: findings from single-cell RNA sequencing.","authors":"Shanhong Fang, Songye Wu, Peng Chen","doi":"10.1038/s41420-025-02359-2","DOIUrl":"10.1038/s41420-025-02359-2","url":null,"abstract":"<p><p>Rotator cuff injury (RCI), a prevalent cause of shoulder pain and disability, often leads to significant functional impairments due to adipocyte infiltration into the damaged tissue. Caveolin-1 (Cav-1), a critical membrane protein, plays a significant role in adipocyte differentiation and lipid metabolism. This study utilized single-cell RNA sequencing (scRNA-seq) to investigate the heterogeneity of cell subpopulations in RCI tissues and assess the regulatory effects of Cav-1. The findings revealed that Cav-1 expression negatively correlates with adipogenic activity, and its modulation through exercise or targeted therapies can significantly reduce adipocyte infiltration and enhance tissue repair. Further, Cav-1 knockout and overexpression models demonstrated the protein's impact on key genes involved in adipocyte differentiation and lipid metabolism, such as Scd1, fatty acid synthase (FASN), and peroxisome proliferator-activated receptor gamma (Pparg). Animal studies corroborated these results, showing that exercise intervention increased Cav-1 expression, decreased adipocyte infiltration, and promoted structural repair. These insights suggest that targeting Cav-1 could offer a novel therapeutic strategy for improving RCI outcomes.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"88"},"PeriodicalIF":6.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566181","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":"Different types of cell death and their interactions in myocardial ischemia-reperfusion injury.","authors":"Bingxin Du, Qiang Fu, Qin Yang, Yeying Yang, Rui Li, Xu Yang, Qingrong Yang, Shuo Li, Jinwei Tian, Huibin Liu","doi":"10.1038/s41420-025-02372-5","DOIUrl":"10.1038/s41420-025-02372-5","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion (I/R) injury is a multifaceted process observed in patients with coronary artery disease when blood flow is restored to the heart tissue following ischemia-induced damage. Cardiomyocyte cell death, particularly through apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis, is pivotal in myocardial I/R injury. Preventing cell death during the process of I/R is vital for improving ischemic cardiomyopathy. These multiple forms of cell death can occur simultaneously, interact with each other, and contribute to the complexity of myocardial I/R injury. In this review, we aim to provide a comprehensive summary of the key molecular mechanisms and regulatory patterns involved in these five types of cell death in myocardial I/R injury. We will also discuss the crosstalk and intricate interactions among these mechanisms, highlighting the interplay between different types of cell death. Furthermore, we will explore specific molecules or targets that participate in different cell death pathways and elucidate their mechanisms of action. It is important to note that manipulating the molecules or targets involved in distinct cell death processes may have a significant impact on reducing myocardial I/R injury. By enhancing researchers' understanding of the mechanisms and interactions among different types of cell death in myocardial I/R injury, this review aims to pave the way for the development of novel interventions for cardio-protection in patients affected by myocardial I/R injury.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"87"},"PeriodicalIF":6.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566179","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}