Cell Death Discovery最新文献

{"title":"ERBB3 influences the ferroptosis pathway via modulation of lipid peroxidation and GSH synthesis in gastric cancer.","authors":"Robert Jenke, Theresa Heinrich, Florian Lordick, Achim Aigner","doi":"10.1038/s41420-025-02707-2","DOIUrl":"10.1038/s41420-025-02707-2","url":null,"abstract":"<p><p>Gastric cancer remains one of the most lethal malignancies worldwide, with high relapse rates and limited survival for patients with advanced disease. Despite advances in targeted therapies and immune checkpoint inhibition, intrinsic tumor heterogeneity poses challenges for effective treatment. The HER3 receptor (ERBB3) has emerged as an important player in cancer progression, contributing to aggressive tumor behavior and poor prognosis. Recent evidence indicates that activating ferroptosis-an iron-dependent, non-apoptotic form of cell death-offers a promising strategy to inhibit cancer growth. In gastric cancer, ferroptosis plays a crucial role, and promoting this process may open new avenues for therapeutic intervention. Ferroptosis is characterized by iron-mediated lipid peroxidation of cell membranes and is critically regulated by the cystine/glutamate antiporter system (SLC7A11) and glutathione peroxidase 4 (GPX4). Our study aimed to investigate the relationship between ERBB3 and ferroptosis in gastric cancer. We found that high ERBB3 expression correlated with resistance to ferroptosis-inducing agents, including GPX4 and SLC7A11 inhibitors, across multiple cell lines. Vice versa, ERBB3 inhibition with TX1-85-1 induced lipid peroxidation in gastric cancer cells, with effects most pronounced in cell lines expressing higher SLC7A11 levels. Knockdown of ERBB3 reproduced these effects, suggesting SLC7A11 as a predictive marker. Importantly, combined inhibition of ERBB3 and GPX4 significantly enhanced lipid peroxidation and cytotoxicity, while ERBB3 activation by co-treatment with the ERBB3 ligand heregulin reduced lipid peroxidation in cells with lower baseline SLC7A11 expression. Analysis of glutathione levels and SLC7A11 expression further supported the role of ERBB3 in modulating ferroptosis sensitivity. These findings identify ERBB3 as a critical regulator of ferroptosis and a promising target for enhancing ferroptosis-mediated cell death. Its inhibition in combination with ferroptosis inducers may thus represent a particularly promising and efficacious therapeutic strategy in gastric cancer.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"398"},"PeriodicalIF":7.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944507","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":"Adipocyte-derived IL6 and triple-negative breast cancer cell-derived CXCL1 co-activate STAT3/NF-κB pathway to mediate the crosstalk between adipocytes and triple-negative breast cancer cells.","authors":"Guo-Tian Ruan, Li-Chen Zhu, Hai-Lun Xie, He-Yang Zhang, Meng-Meng Song, Li Deng, Han-Ping Shi","doi":"10.1038/s41420-025-02713-4","DOIUrl":"10.1038/s41420-025-02713-4","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is correlated to a poor prognosis, especially in the context of obesity. The interaction between adipocytes and TNBC cellsplay a key role in the progression of TNBC. This study aims to investigate the mechanisms underlying the cross-talk and progression between adipocytes and TNBC cells. We established a co-culture model involving mature adipose cells (hADSC and 3T3-L1) and TNBC cells. Cell invasion abilities were assessed using wound healing and Transwell assays. Gene and protein expression levels were examined using RT-PCR, western blotting, and immunostaining. Adipocytokine and chemokine levels were measured using ELISA. Additionally, we developed a fat mouse model induced by a high-fat diet and a tumor-bearing model of TNBC cells in vivo. The results indicated a significant enhancement in the invasion abilities of TNBC cells after co-culture. Mature adipose tissue co-cultured with TNBC cells increased the expression and secretion of C-X-C motif chemokine ligand 1 (CXCL1) and upregulated matrix metalloproteinase 7 (MMP7) and MMP9 in TNBC cells by activating the signal transducer and activator of transcription 3 (STAT3) /nuclear factor-κB p65 (NF-κB p65) pathway. Additionally, co-culture activated the STAT3/NF-κB p65 pathway, increasing the expression and secretion of IL6 in adipocytes. Based on the mouse obesity model, our experiments on orthotopic breast fat pad xenoimplantation showed consistent results in vivo. Our findings suggest a cross-talk between TNBC cells and adipocytes, activating the STAT/NF-κB p65 pathway through the production and secretion of CXCL1 and IL6, respectively, thereby promoting TNBC progression. These results propose a potential strategy for developing individualized treatments for patients with TNBC in clinical practice.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"395"},"PeriodicalIF":7.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12370983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944404","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":"Phospholipid scramblase 1 (PLSCR1) is a novel substrate of NEDD4-2 (NEDD4L) mediated ubiquitination.","authors":"Meriam Shabbar, Jantina A Manning, Yoon Lim, Sonia S Shah, Diva Sinha, Andrej Nikolic, Jarrod J Sandow, Sharad Kumar","doi":"10.1038/s41420-025-02700-9","DOIUrl":"10.1038/s41420-025-02700-9","url":null,"abstract":"<p><p>NEDD4-2 (human NEDD4L), a ubiquitin ligase, plays an essential role in regulating a number of membrane proteins, including ion channels and transporters. In the kidney, NEDD4-2 deletion results in a progressive loss of tubular cells and salt-sensitive chronic kidney disease. While deregulation of sodium homeostasis due to increased levels and function of the epithelial sodium channel (ENaC) and sodium chloride transporter (NCC), both NEDD4-2 substrates, plays a critical role in kidney damage in this model, other ubiquitination targets may also be important. Here, we employed an affinity purification mass spectrometry approach to identify additional interactors of NEDD4-2 in kidney cells and discovered phospholipid scramblase 1 (PLSCR1) as a new NEDD4-2 substrate. We show that PLSCR1 is a direct interactor and substrate of NEDD4-2. As a result, NEDD4-2 deficiency both in cultured cells and in mouse kidney resulted in increased levels of PLSCR1 protein. We observed increased phosphatidyl serine exposure in NEDD4-2 knockout cells in response to both calcium and apoptotic stimuli and this phenotype was reversed when NEDD4-2 expression was restored. Consistently, apoptotic cells lacking NEDD4-2 showed a higher rate of macrophage clearance. Together, these results indicate that PLSCR1 is a novel substrate of NEDD4-2-mediated ubiquitination and that NEDD4-2 regulates PLSCR1 protein stability and function.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"393"},"PeriodicalIF":7.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12368045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944511","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":"Nitroxoline is a novel inhibitor of NLRP3-dependent pyroptosis.","authors":"Christina Maeder, Roberto Baumann, Susanne Gaul, Sven Fikenzer, Michael Schaefer, Hermann Kalwa, Ulrich Laufs, Alexander Kogel","doi":"10.1038/s41420-025-02699-z","DOIUrl":"10.1038/s41420-025-02699-z","url":null,"abstract":"<p><p>Aberrant activity of the NLR family pyrin domain containing 3 (NLRP3) inflammasome contributes to a wide range of diseases associated with acute inflammatory responses and chronic sterile inflammation. Activation of the NLRP3 inflammasome mediates pyroptotic cell death and the release of pro-inflammatory cytokines. To date, no selective inhibitor of inflammasome activity is available for the use in humans. We conducted a medium-throughput screening of 6280 drugs or drug-like compounds and identified novel inhibitors of the NLRP3 inflammasome. Among these, nitroxoline was further characterized because the drug is approved for antibiotic treatment in humans, and we found no toxicity over a wide range of concentrations. Treatment of THP-1 monocytes with 80 μM nitroxoline markedly reduced the secretion of the pro-inflammatory cytokine Interleukin-1β (IL-1β) by 95% from 197.8 pg ml^-1 to 11.0 pg ml^-1. Nitroxoline reduced downstream events of inflammasome activation including caspase-1 activity (FAM-Flica⁺/7AAD⁺ cells control 57.1 ± 9.4% vs. nitroxoline 27.9 ± 15.5%) and gasdermin D cleavage (ratio cleaved/uncleaved control 8.7 ± 4.3 vs. nitroxoline 1.3 ± 1.3, p < 0.05). The data were confirmed in cultured human PBMC, where nitroxoline abrogated IL-1β secretion. Mechanistically, drug affinity-responsive target assays revealed that nitroxoline directly interacts with the NACHT domain of NLRP3, inhibiting inflammasome assembly. Nitroxoline did not affect NF-κB-dependent gene expression, as analyzed by nuclear p65 translocation and IκBα phosphorylation, and did not inhibit the NLR-family member NLRC4 or the AIM2 inflammasomes, indicating specificity for NLRP3. Nitroxoline is a novel inhibitor of the NLRP3 inflammasome, which reduces inflammasome assembly and IL-1β release. These data set the stage for testing the effects of nitroxoline on sterile inflammation in clinical studies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"394"},"PeriodicalIF":7.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12368067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944567","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":"Exploring the metabolic signaling network of GFPT in cancer.","authors":"Chibuzo Sampson, Pengfei Li, Yiqian Wang, Jing Liu, Jing Lv, Tian Xia, Hai-Long Piao, Yegang Ma","doi":"10.1038/s41420-025-02687-3","DOIUrl":"10.1038/s41420-025-02687-3","url":null,"abstract":"<p><p>Metabolic homeostasis is essential for cellular function in living organisms. In cancer cells, metabolic processes are reprogrammed to meet the energy demands and biosynthetic needs for rapid growth. This reprogramming enhances nutrient flux through the glycolytic pathway, supporting ATP production and branching into pathways that synthesize macromolecules required for cell proliferation. One critical branching pathway is the hexosamine biosynthesis pathway (HBP), which, driven by metabolic reprogramming, facilitates the synthesis of uridine-5'-diphospho-N-acetylglucosamine (UDP-GlcNAc), a glycosylation substrate. This pathway is regulated by the rate-limiting enzyme glutamine-fructose-6-phosphate transaminase (GFPT), a key controller of cellular UDP-GlcNAc levels and protein glycosylation. Dysregulation of GFPT is linked to metabolic disorders, like in diabetes, and it is also frequently upregulated in cancers. Given that GFPT plays a pivotal role in cancer metabolism, elucidating its regulatory interactions with other metabolic signaling pathways under metabolic stress is crucial to identifying therapeutic vulnerabilities in cancer. This review discusses the interaction network of GFPT with other metabolic pathways, its role in nutrient sensing, and the implications of GFPT deregulation in cancer.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"388"},"PeriodicalIF":7.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882298","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":"Discovery of a novel potent tubulin inhibitor through virtual screening and target validation for cancer chemotherapy.","authors":"Peipei Shan, Kai-Lu Liu, Xiu Jiang, Guangzhao Zhou, Kongkai Zhu, Hua Zhang","doi":"10.1038/s41420-025-02679-3","DOIUrl":"10.1038/s41420-025-02679-3","url":null,"abstract":"<p><p>Microtubules, critical to diverse cellular processes, represent a clinically validated target for anticancer therapeutics. In this study, a virtual screening of the Specs library, consisting of 200,340 compounds, was conducted to target the taxane and colchicine binding sites on tubulin, resulting in the identification of 93 promising candidates for further analysis. Subsequent characterization revealed a nicotinic acid derivative (compound 89) as a potent tubulin inhibitor, demonstrating significant anti-tumor efficacy in vitro and in vivo, with no observable toxicity at therapeutic doses in mice. Notably, compound 89 also exhibited robust antitumor activity in patient-derived organoids. Mechanistic studies, including EBI competitive binding assays and molecular docking, confirmed its inhibition toward tubulin polymerization via selective binding to the colchicine site. Furthermore, compound 89 disrupted tubulin assembly dynamics through modulation of the PI3K/Akt signaling pathway. This work presents a novel tubulin-inhibiting scaffold with potential for advancing next-generation microtubule-targeted chemotherapies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"392"},"PeriodicalIF":7.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882295","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":"Diverse functions of NLRP3 inflammasome in PANoptosis and diseases.","authors":"Yuanyuan Jiang, Zhiyuan Qiang, Yue Liu, Liwei Zhu, Long Xiao, Zhenfang Du, Rong Cai, Sheng Qiang","doi":"10.1038/s41420-025-02689-1","DOIUrl":"10.1038/s41420-025-02689-1","url":null,"abstract":"<p><p>NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) is a vital sensor of the innate immune system, capable of responding to various exogenous invading pathogens and endogenous cell injury. Once the danger signal is detected, NLRP3 recruits downstream molecules to assemble into inflammasomes, which induce inflammatory cell death and trigger an inflammatory response. PANoptosis is a specific mode of inflammatory cell death that integrates the processes of pyroptosis, apoptosis, and necrosis. It is primarily driven by a multiprotein complex termed the PANoptosome. The NLRP3 inflammasome, an essential component of the PANoptosome, is implicated in the pathogenesis of several human disorders. Targeted inhibition of NLRP3 activation specifically has a notable impact on mitigating a variety of disease conditions. This review briefly describes how the NLRP3 inflammasome forms and is activated, outlines its multifaceted roles in disorders, and emphasizes the vital role of NLRP3 in PANoptosis. Additionally, we discuss the potential of NLRP3 as a target for the clinical management of associated diseases. Improved understanding of the NLRP3 inflammasome and its involvement in PANoptosis is crucial for guiding new treatment strategies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"389"},"PeriodicalIF":7.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882296","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":"The ATF4-glutamine axis: a central node in cancer metabolism, stress adaptation, and therapeutic targeting.","authors":"Xing Yan, Changhong Liu","doi":"10.1038/s41420-025-02683-7","DOIUrl":"10.1038/s41420-025-02683-7","url":null,"abstract":"<p><p>At the center of tumor(neoplasm) metabolic adaptation lies activating transcription factor 4 (ATF4), a key regulator that orchestrates Glutamine (Gln) uptake, utilization, and redox balance under conditions of nutrient deprivation and oxidative stress. This review explores how ATF4 integrates environmental and cellular stress signals to drive Gln metabolic processes, enabling tumor survival, metabolic reprogramming, and immune evasion. The ATF4-Gln axis emerges as a pivotal vulnerability in cancer metabolic processes. Preclinical studies of small-molecule inhibitors and synthetic derivatives disrupting this pathway show promising results. Understanding the intricate interplay between ATF4, Gln metabolic processes, and cancer progression provides valuable insights for novel therapeutic strategies. Future research must address tumor heterogeneity and metabolic flexibility to fully harness the potential of ATF4-centered therapies. However, challenges such as off-target effects of ATF4 inhibitors and metabolic plasticity in tumors remain critical barriers. Future studies integrating multi-omics approaches and AI-driven drug discovery are warranted to overcome these hurdles.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"390"},"PeriodicalIF":7.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882299","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":"Emerging implications of N6-methyladenosine in prostate cancer progression and treatment.","authors":"Junyan Xu, Dajun Gao, Changjie Ren, Zhong Wang, Fuwen Yuan, Yanting Shen","doi":"10.1038/s41420-025-02680-w","DOIUrl":"10.1038/s41420-025-02680-w","url":null,"abstract":"<p><p>RNA modifications are widely distributed in almost all types of RNA, including mRNA, rRNA, miRNA, circRNA, and lncRNA, which are deeply involved in disease initiation and progression and are emerging therapeutic targets in diseases such as cancer, among which N6-methyladenosine (m6A) is the most abundant mRNA modification. Accumulating studies have demonstrated the critical role of m6A during cancer progression and its therapeutic potential in prostate cancer, which is one of the most common malignancies in men worldwide. Here, we reviewed the emerging roles of m6A regulators, including readers, writers, and erasers, and the downstream m6A-modified mRNA and noncoding RNA in prostate cancer. We also discussed the therapeutic potential of targeting m6A in prostate cancer and summarized the emerging agents and technologies, such as the cutting-edge CRISPR-Cas13 in prostate cancer treatment by targeting m6A regulatory pathways. At last, we elucidated the perspective of developing efficient and specific RNA targeting agents and technological platforms to provide new strategies for treating prostate cancer by targeting RNA modifications.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"391"},"PeriodicalIF":7.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882297","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":"Epigenetic control in thyroid cancer: mechanisms and clinical perspective.","authors":"Jiahui Zhang, Shengkai Zheng, Ruiwang Xie, Junsi Zhang, Xiangjin Chen, Sunwang Xu","doi":"10.1038/s41420-025-02688-2","DOIUrl":"10.1038/s41420-025-02688-2","url":null,"abstract":"<p><p>Epigenetic regulation plays a key role in the progression, proliferation, and dedifferentiation of thyroid cancer. Epigenetic control occurs at multiple levels, including DNA methylation, RNA modification, histone modification, chromatin remodeling, and chromatin accessibility. Genetic alterations in chromatin regulators are commonly observed in thyroid cancer, which includes papillary thyroid carcinoma (PTC), medullary thyroid carcinoma (MTC), anaplastic thyroid carcinoma (ATC), and follicular thyroid carcinoma (FTC). These cancers exhibit distinct characteristics in terms of genetics, biology, and clinical presentation. Therefore, we review the disease biology driven by changes in chromatin pathways in thyroid cancer. Specifically, we summarize examples of epigenetic dysregulation at each level, with mechanisms involving alterations in enzymes regulating DNA methylation, RNA modification and posttranslational modifications of histones, as well as the loss or fusion of subunits involved in chromatin remodeling and chromatin accessibility. Finally, on the basis of clinical applications, we review the current and potential future approaches for thyroid cancer treatment.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"387"},"PeriodicalIF":7.0,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862118","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}