Cell Death Discovery最新文献

{"title":"Single-cell RNA sequencing revealed cell landscape of tongue dorsal mucosa in rats with gastric intestinal metaplasia.","authors":"Jiao Xiang, Jing Han, Jianping Wu, Shuo Xu, Chun Cheng, Junfeng Zhang","doi":"10.1038/s41420-025-02386-z","DOIUrl":"10.1038/s41420-025-02386-z","url":null,"abstract":"<p><p>The formation of tongue coating is closely related with the differentiation of the lingual dorsal mucosa, and a great deal of evidence shows that the variation of tongue coating reflects the pathological and physiological state of the gastric mucosa. However, the detailed mechanism remains elusive. This study established a rat model of gastric intestinal metaplasia (GIM) with 2% sodium salicylate and 20 mmol/L of deoxycholate sodium, and used single-cell RNA sequencing (scRNA-seq) to reveal the cell landscape of tongue dorsal mucosa. In comparison to the control group, the tongue dorsal mucosa of GIM rats became grayish-white, and the histologic characteristics presented an uneven distribution of tongue papilla with many immune cells in the submucosal layer. The expressive levels of pro-inflammatory factors (IL-1β, IL-6, and IL-17) were significantly higher in GIM rats than in the control group. Stratified analysis revealed the significant downregulation of autophagy marker gene Map1lc3a in neutrophils and T cells, and the significant downregulation of cuproptosis marker gene Dlst in fibroblasts of the tongue dorsal mucosa in GIM rats. These changes were closely related to mucosal inflammation and impaired tissue barrier integrity. Significantly, the expression of several keratin genes (Krt7, Krt8, Krt13, Krt16, and Krt76) was significantly downregulated, as well as the expression of the bitter taste receptor gene Rtp4 and the sweet taste receptor gene Tas1r2 in the GIM rats. The data indicated that fewer cells entered regulated cell death in immune cells of tongue mucosa, a more active inflammatory response occurred, the keratinization of tongue dorsal mucosal cells was inhibited, and the taste perception function was weakened. The results bring new perspectives on tongue coating in the application of gastric disorders. Characteristics of the tongue dorsum mucosal cell landscape in the rats with gastric intestinal metaplasia. The abundances of T cells, neutrophils, and macrophages were upregulated, and the autophagy marker gene Map1lc3a in T cells and neutrophils was downregulated, which indicated an actively inflammatory immune response. Downregulation of cuprotosis marker gene Dlst in fibroblasts suggested potential damage to the mucosal barrier. Meanwhile, the expression of bitter receptor Rtp4 and sweet receptor Tas1r2 in mesenchymal stem cells was downregulated. The cell communication ability was reduced, especially between mesenchymal stem cells and epithelial cells. In a word, the abnormal status of tongue dorsum mucosa may accompany the development of gastric intestinal metaplasia.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"105"},"PeriodicalIF":6.1,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647344","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":"Investigating synthetic lethality and PARP inhibitor resistance in pancreatic cancer through enantiomer differential activity.","authors":"Mirco Masi, Laura Poppi, Viola Previtali, Shannon R Nelson, Kieran Wynne, Giulia Varignani, Federico Falchi, Marina Veronesi, Ennio Albanesi, Daniele Tedesco, Francesca De Franco, Andrea Ciamarone, Samuel H Myers, Jose Antonio Ortega, Greta Bagnolini, Giovanni Ferrandi, Fulvia Farabegoli, Nicola Tirelli, Giuseppina Di Stefano, Giorgio Oliviero, Naomi Walsh, Marinella Roberti, Stefania Girotto, Andrea Cavalli","doi":"10.1038/s41420-025-02382-3","DOIUrl":"10.1038/s41420-025-02382-3","url":null,"abstract":"<p><p>The RAD51-BRCA2 interaction is central to DNA repair through homologous recombination. Emerging evidence indicates RAD51 overexpression and its correlation with chemoresistance in various cancers, suggesting RAD51-BRCA2 inhibition as a compelling avenue for intervention. We previously showed that combining olaparib (a PARP inhibitor (PARPi)) with RS-35d (a BRCA2-RAD51 inhibitor) was efficient in killing pancreatic ductal adenocarcinoma (PDAC) cells. However, RS-35d impaired cell viability even when administered alone, suggesting potential off-target effects. Here, through multiple, integrated orthogonal biological approaches in different 2D and 3D PDAC cultures, we characterised RS-35d enantiomers, in terms of mode of action and single contributions. By differentially inhibiting both RAD51-BRCA2 interaction and sensor kinases ATM, ATR and DNA-PK, RS-35d enantiomers exhibit a 'within-pathway synthetic lethality' profile. To the best of our knowledge, this is the first reported proof-of-concept single small molecule capable of demonstrating this built-in synergism. In addition, RS-35d effect on BRCA2-mutated, olaparib-resistant PDAC cells suggests that this compound may be effective as an anticancer agent possibly capable of overcoming PARPi resistance. Our results demonstrate the potential of synthetic lethality, with its diversified applications, to propose new and concrete opportunities to effectively kill cancer cells while limiting side effects and potentially overcoming emerging drug resistance.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"106"},"PeriodicalIF":6.1,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647328","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":"METTL3-m⁶A-mediated TGF-β signaling promotes Fuchs endothelial corneal dystrophy via regulating corneal endothelial-to-mesenchymal transition.","authors":"Jini Qiu, Xueling Zhang, Qian Shi, Yujing Yang, Rongmei Zhou, Jun Xiang, Jiayu Gu, Jianjiang Xu, Jiaxu Hong, Kun Shan","doi":"10.1038/s41420-025-02384-1","DOIUrl":"10.1038/s41420-025-02384-1","url":null,"abstract":"<p><p>Fuchs endothelial corneal dystrophy (FECD) is the leading cause of vision-threatening corneal endothelial dystrophy without pharmacologic treatments. Corneal endothelial-mesenchymal transition (cEndMT), a specific cellular phenotypic transition, is implicated in the vicious cycle in FECD pathogenesis. Here, we investigated the reversible epigenetic regulation of N⁶-methyladenosine (m⁶A) during cEndMT process and FECD progression. The m⁶A writer methyltransferase-like 3 (METTL3) was significantly upregulated in FECD models and induced transcriptomic hypermethylation, including TGFB2 mRNA. METTL3 promoted the translation of hypermethylated TGFB2 mRNA in an YTHDF1-dependent manner, resulting in upregulation of TGF-β2 protein and activation of TGF-β signaling. Intervention of METTL3 expression or catalytic activity could suppress TGF-β signaling activation, subsequently ameliorate cEndMT process and FECD progression. This study reveals unique METTL3-m⁶A-mediated mechanism in regulating cEndMT process, suggesting the prevailing role of m⁶A in cellular phenotypic transition. Targeting METTL3/m⁶A is a promising strategy for FECD treatment. Schematic representation of METTL3-m⁶A-TGF-β signaling regulating FCED. In the context of environmental stress, METTL3 is upregulated in corneal endothelium, which in turn leads to increased m⁶A level of TGFB2 mRNA, upregulation of TGF-β2 protein via YTHDF1 mechanism, and activation of TGF-β signaling pathway. The regulation of these mechanisms results in the progressive irreversible transition of corneal endothelial cells from their specific phenotype to a mesenchymal phenotype, which accelerates the progression of FECD.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"104"},"PeriodicalIF":6.1,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633741","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":"Lentinan suppresses the progression of neuroblastoma by inhibiting FOS-mediated transcription activation of VRK1 to stabilize p53 protein.","authors":"Zhang Zhao, Jiahao Li, Liyu Zhang, Jiayu Wang, Dian Li, Manna Zheng, Zijie Ye, Tianyou Yang, Yan Zou, Jing Pan, Hui Xu, Huijuan Zeng, Chao Hu","doi":"10.1038/s41420-025-02315-0","DOIUrl":"10.1038/s41420-025-02315-0","url":null,"abstract":"<p><p>Neuroblastoma (NB) is a common malignant and solid pediatric tumor with unfavorable prognosis. Although studies have shown the anti-tumor efficacy of lentinan (LNT), molecular mechanism that contribute to the anti-tumor effect on NB remains unclear. The aim of this study is to unmask the anti-tumor role of LNT in NB and the specific molecular mechanism. At first, the in vivo experiments were conducted and the results indicated that LNT could suppress tumor growth in NB. Subsequent cellular functional assays unveiled that LNT treatment could efficiently decrease NB cell viability, induce cell cycle stagnation at G0/G1 phase, increase the apoptosis rate, and weaken the migrating and invasive abilities. Furthermore, LNT resulted in a significant downregulation of FOS expression. FOS overexpression recovered the growth, migration and invasion of NB cells suppressed by LNT treatment. Mechanism investigations revealed that FOS interacted with JUND to transcriptionally activate VRK1. Moreover, VRK1 downregulated p53 protein via inducing the phosphorylation of p53 at site 291-393. In summary, this study reveals a novel molecular pathway by which LNT exerts tumor-suppressing functions in NB.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"103"},"PeriodicalIF":6.1,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633740","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":"Basic biology and roles of CEBPD in cardiovascular disease.","authors":"Tongjun Li, Shaoling Lin, Yingyin Zhu, Dewei Ye, Xianglu Rong, Lexun Wang","doi":"10.1038/s41420-025-02357-4","DOIUrl":"10.1038/s41420-025-02357-4","url":null,"abstract":"<p><p>CCAAT/enhancer-binding protein delta (CEBPD), as an evolutionarily conserved protein in mammals, belongs to the CEBP transcription factor family, which modulates many biological processes. The diversity of CEBPD functions partly depends on the cell type and cellular context. Aberrant CEBPD expression and activity are associated with multiple organ diseases, including cardiovascular diseases. In this review, we describe the basic molecular biology of CEBPD to understand its expression regulation, modifications, and functions. Here, we summarize the recent advances in genetically modified animals with CEBPD. Finally, we discuss the contribution of CEBPD to cardiovascular diseases and highlight the strategies for developing novel therapies targeting CEBPD.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"102"},"PeriodicalIF":6.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633737","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":"Lactylation: a promising therapeutic target in ischemia-reperfusion injury management.","authors":"Fei-Xiang Wang, Guo Mu, Zi-Hang Yu, Zu-An Shi, Xue-Xin Li, Xin Fan, Ye Chen, Jun Zhou","doi":"10.1038/s41420-025-02381-4","DOIUrl":"10.1038/s41420-025-02381-4","url":null,"abstract":"<p><p>Ischemia-reperfusion injury (IRI) is a critical condition that poses a significant threat to patient safety. The production of lactate increases during the process of IRI, and lactate serves as a crucial indicator for assessing the severity of such injury. Lactylation, a newly discovered post-translational modification in 2019, is induced by lactic acid and predominantly occurs on lysine residues of histone or nonhistone proteins. Extensive studies have demonstrated the pivotal role of lactylation in the pathogenesis and progression of various diseases, including melanoma, myocardial infarction, hepatocellular carcinoma, Alzheimer's disease, and nonalcoholic fatty liver disease. Additionally, a marked correlation between lactylation and inflammation has been observed. This article provides a comprehensive review of the mechanism underlying lactylation in IRI to establish a theoretical foundation for better understanding the interplay between lactylation and IRI.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"100"},"PeriodicalIF":6.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623779","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":"m6A-modified LINC02418 induces transcriptional and post-transcriptional modification of CTNNB1 via interacting with YBX1 and IGF2BP1 in colorectal cancer.","authors":"Hao Zhang, Ye Han, Chengwei Wu, Siying Wang, Mingquan Chen, Qian Xu, Hong Wei, Xianli Zhou, Guiyu Wang","doi":"10.1038/s41420-025-02365-4","DOIUrl":"10.1038/s41420-025-02365-4","url":null,"abstract":"<p><p>Colorectal cancer (CRC) represents a significant menace to human health, but its molecular pathogenesis remains unclear. Herein, we explored the functional role of LINC02418 in CRC progression. The function of LINC02418 in CRC was determined through vitro and in vivo experiments. The molecular mechanism of LINC02418 in CRC was explored by quantitative real-time PCR (qPCR) analyses, western blot, luciferase reporter assay, methylated RNA immunoprecipitation (MeRIP) assay, RNA pull-down, RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay. The results revealed that LINC02418 expression was upregulated in CRC tissues and the high expression of LINC02418 was related to unfavorable survival of CRC patients. Besides, knockdown of LINC02418 expression resulted in the inhibition of proliferation and metastasis of CRC cells in vitro and in vivo. Mechanistically, we found METTL3-mediated m6A modification induced the aberrant expression of LINC02418 in CRC. LINC02418 could interact with YBX1 and enhance YBX1 DNA-binding ability to the CTNNB1 promoter, resulting in transcriptional activation of CTNNB1. In the post-transcriptional stage, LINC02418 could also enhance CTNNB1 stability by promoting the interaction between IGF2BP1 protein and CTNNB1 mRNA. What is more, LINC02418 expression could be transcriptionally enhanced by YBX1 protein. Collectively, this study unveils a novel oncogenic mechanism for LINC02418 in CRC and the LINC02418 might be a novel therapeutic target in CRC treatment.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"101"},"PeriodicalIF":6.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623812","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":"Deficiency of UBE3D in mice leads to severe embryonic abnormalities and disrupts the mRNA of Homeobox genes via CPSF3.","authors":"Yiwei Mi, Lu Yan, Yu Wu, Yufang Zheng","doi":"10.1038/s41420-025-02387-y","DOIUrl":"10.1038/s41420-025-02387-y","url":null,"abstract":"<p><p>Neurulation is a crucial event during vertebrate early embryogenesis, and abnormalities in this process can result in embryonic lethality or congenital disorders, such as neural tube defects. Through our previous phenotypic-driven screening in mice, we have identified UBE3D as a key factor for the neurulation process. By generating Ube3d knockout mice using CRISPR/Cas9 technology, we observed that homozygous mice exhibited severe growth retardation and malformation, ultimately dying between E10.5 to E11.5. In contrast to their wild-type and heterozygote littermates, homozygous embryos displayed small heads and unturned caudal neural tubes at E9.5. Our in situ hybridization and immunofluorescence experiments revealed high expression of UBE3D in the forebrain, neural tube, and heart at E9.5-10.5. Furthermore, RNA-seq analysis of the E10.5 embryos demonstrated that deficiency in UBE3D resulted in the downregulation of multiple Homeobox genes, including those specifically expressed in the forebrain and lumbosacral regions. We also discovered that UBE3D interacts with CPSF3, which is an endonuclease essential for the pre-mRNA 3' end process. UBE3D could de-ubiquitinate CPSF3, and a deficiency of UBE3D leads to reduced levels of CPSF3 in both mouse and human cells. Overexpression of dominant negative mutants of CPSF3 was found to partially reduce mRNA levels of several Homeobox genes. In summary, our findings highlight that UBE3D is critical for early embryonic development in mice.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"99"},"PeriodicalIF":6.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613685","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 feedback loop between miR-222-3p and ZEB1 harnesses metastasis in renal cell carcinoma.","authors":"Fan Wang, Liao Li, Xiangfu Sun, Xianfu Cai, Jianjun Wang, Huiwen Luo, Yaodong Wang, Dong Ni, Decai Wang","doi":"10.1038/s41420-025-02385-0","DOIUrl":"10.1038/s41420-025-02385-0","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC) is an aggressive malignancy originating from the renal parenchyma, often leading to high mortality due to local invasion and distant metastasis. MicroRNAs (miRNAs) play essential roles in RCC progression. Through miRNA sequencing, we identified significant upregulation of miR-222-3p in metastatic RCC tissues. Exosomes from highly metastatic RCC cells were found to transfer miR-222-3p to low-metastatic cells, enhancing their migration and invasion. Mechanistically, miR-222-3p directly targets the 3' untranslated region (3'UTR) of the tumor-suppressor TRPS1, reducing its expression. TRPS1 downregulation releases its inhibitory effect on ZEB1, a key regulator of epithelial-mesenchymal transition (EMT), thereby promoting EMT and metastatic traits. ZEB1 further transactivates miR-222-3p, establishing a positive feedback loop. Additionally, miR-222-3p promotes a pre-metastatic niche by inducing M2 macrophage polarization, facilitating distant metastasis. These findings highlight miR-222-3p as a critical driver of RCC metastasis and suggest its potential as a diagnostic marker and therapeutic target for RCC.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"97"},"PeriodicalIF":6.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613695","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":"Replication stress promotes cellular transformation in Drosophila epithelium.","authors":"Maria Molano-Fernández, Ian D Hickson, Héctor Herranz","doi":"10.1038/s41420-025-02383-2","DOIUrl":"10.1038/s41420-025-02383-2","url":null,"abstract":"<p><p>The accurate control of DNA replication is crucial for the maintenance of genomic stability and cell viability. In this study, we explore the consequences of depleting the replicative DNA Polymerase α (POLA) in the wing disc of Drosophila melanogaster. Our findings reveal that reduced POLA activity induces DNA replication stress and activates the replication checkpoint in vivo. Consistent with this, we demonstrate that dATR, a key component in DNA replication checkpoint signaling, is essential for the maintenance of tissue integrity under conditions of compromised POLA activity. We show that cells within the wing disc exhibiting reduced POLA activity arrest in the G2 phase and undergo p53-dependent apoptosis. We also reveal a critical role for DNA Ligase 4 in sustaining cell viability when POLA function is impaired. Most notably, we report the appearance of oncogenic traits in wing disc cells with diminished POLA activity when apoptosis is suppressed. In this context, the overexpression of the oncogene cdc25/string enhances the oncogenic phenotype. These results indicate that a combination of oncogenic activation, replication stress, and suppression of apoptosis is sufficient to promote the emergence of hallmarks of tumorigenesis, highlighting major implications for cancer development in humans.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"96"},"PeriodicalIF":6.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613686","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}