Cellular and Molecular Life Sciences最新文献

{"title":"Correction to: Knockdown of Foxg1 in supporting cells increases the trans‑differentiation of supporting cells into hair cells in the neonatal mouse cochlea.","authors":"Shasha Zhang, Yuan Zhang, Ying Dong, Lingna Guo, Zhong Zhang, Buwei Shao, Jieyu Qi, Han Zhou, Weijie Zhu, Xiaoqian Yan, Guodong Hong, Liyan Zhang, Xiaoli Zhang, Mingliang Tang, Chunjie Zhao, Xia Gao, Renjie Chai","doi":"10.1007/s00018-026-06289-9","DOIUrl":"10.1007/s00018-026-06289-9","url":null,"abstract":"","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"83 1","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13379533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469267","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":"Upregulation of PTPRO by WT1 alleviates podocyte injury in diabetic nephropathy through inhibiting the c-Abl/p53 pathway.","authors":"Hengjiang Guo, Li Wang, Yiru Tong, Yan Jiang, Xingmei Yao, Limin Lu, Rong Wei","doi":"10.1007/s00018-026-06343-6","DOIUrl":"10.1007/s00018-026-06343-6","url":null,"abstract":"<p><p>Podocyte injury plays a central role in the pathogenesis of diabetic nephropathy (DN). Protein tyrosine phosphatase receptor type O (PTPRO) has been implicated in glomerular disease, yet its specific role and regulatory mechanism in DN remain poorly understood. Here, we demonstrated that PTPRO expression was significantly downregulated in the glomeruli of DN mice and patients with DN, as well as in cultured podocytes exposed to diabetic stressors. Functional studies revealed that Ptpro knockdown induced podocyte injury, characterized by reduced Nephrin and Podocin expression, increased apoptosis, actin cytoskeleton disruption, enhanced migration, and reduced adhesion. Conversely, PTPRO overexpression ameliorated high glucose (HG)-induced podocyte damage. Mechanistically, PTPRO interacted with and dephosphorylated c-Abl, thereby suppressing the c-Abl/p53 signaling pathway. Pharmacological activation of c-Abl abolished the protective effects of PTPRO. Furthermore, we identified PTPRO as a direct transcriptional target of WT1, a podocyte master transcription factor downregulated in DN. WT1 overexpression restored PTPRO expression, suppressed c-Abl/p53 signaling, and ameliorated HG-induced podocyte injury in vitro. In vivo, podocyte-specific overexpression of WT1 via adeno-associated virus delivery in db/db mice attenuated proteinuria, glomerulosclerosis, and podocyte foot process effacement, accompanied by restored PTPRO expression and inhibition of the c-Abl/p53 pathway. Collectively, these findings establish that PTPRO functions downstream of WT1 to protect podocytes in DN by suppressing c-Abl/p53 signaling. Targeting the WT1-PTPRO-c-Abl-p53 axis may represent a novel therapeutic strategy for DN.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469279","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":"Vestibular hair cell redundancy and the critical requirement of type I cells for balance maintenance.","authors":"Yikang Huang, Wenli Ni, Qin Zhou, Mingchuan Feng, Tao Jiang, Shunji He, Yan Chen, Wenyan Li","doi":"10.1007/s00018-026-06348-1","DOIUrl":"10.1007/s00018-026-06348-1","url":null,"abstract":"<p><p>Vestibular hair cells (HCs) are sensory mechanotransducers essential for balance and spatial orientation, yet the relative contributions of HC number and subtype to vestibular function remain unresolved. Here, we developed a dose-dependent injury model in adult Pou4f3^DTR mice by administering diphtheria toxin (DT), which induced selective HC ablation across vestibular organs. Both type I and type II HCs were lost following DT treatment. Type II HCs exhibited higher susceptibility to DT at lower doses, although this difference diminished as DT dose increased and overall HC survival declined. Functional analyses revealed that mice retaining ~ 30% of vestibular HCs-with preserved subtype proportions and neural innervation-exhibited normal balance, while ~ 50% residual HCs were sufficient to maintain intact vestibulo-ocular reflexes. To elucidate subtype-specific roles, we employed two type I HC-deficient models: 3,3'-iminodipropionitrile-induced injury and Gfi1^Cre/Atoh1-OE mice. Comparative analyses revealed that type I HCs were essential for vestibular function. Together, these findings establish a reliable injury model, demonstrate functional redundancy within vestibular HCs, and underscore the critical role of type I HCs. These insights suggest that efforts to restore vestibular function through HC regeneration should prioritize generating functional type I HCs, not merely increasing the total HC count.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469308","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":"ENO3-mediated glycolytic reprogramming participates in β-glucan-induced dendritic cells activation and anti-tumor responses.","authors":"Jun Ding, Yongzhe Hao, Meng Yuan, Jie Pan, Yewen Xie, Xiao Sun, Yongling Ning, Chunjian Qi","doi":"10.1007/s00018-026-06350-7","DOIUrl":"10.1007/s00018-026-06350-7","url":null,"abstract":"<p><p>Dendritic cells (DCs) are key initiators of antitumor immunity, yet the metabolic drivers governing their activation remain incompletely defined. Here, we show that the fungal immunomodulator β-glucan induces robust immune-metabolic reprogramming in bone marrow-derived DCs (BMDCs), characterized by coordinated increases in glycolysis and tricarboxylic acid cycle activity. This metabolic shift is essential for BMDCs activation, as inhibition of glycolysis or oxidative metabolism diminishes β-glucan-induced costimulatory molecule expression, proinflammatory cytokine production and T-cell priming. Multi-omics profiling identifies enolase 3 (ENO3) as a key glycolytic regulator selectively upregulated by β-glucan. ENO3 knockdown reduces glycolytic flux, decreases mitochondrial ATP and ROS production, and consequently impairs BMDCs maturation and CD8⁺ T-cell responses. In DC-specific ENO3-knockout mice, ENO3 deficiency significantly compromises the antitumor efficacy of β-glucan, which characterized by accelerated tumor growth, impaired DCs activation, reduced CD8⁺ T-cell infiltration, and an immunosuppressive tumor milieu. These findings reveal ENO3 as a critical metabolic regulator linking β-glucan sensing to DC-mediated antitumor immunity.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469269","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":"Molecular mechanisms and translational implications in apoptosis, ferroptosis, pyroptosis, and cuproptosis of spermatogonial stem cells.","authors":"Feng Deng, Jianghong Xiang, Zuping He","doi":"10.1007/s00018-026-06337-4","DOIUrl":"10.1007/s00018-026-06337-4","url":null,"abstract":"<p><p>Spermatogonial stem cells (SSCs) are essential for male fertility because they form the cellular foundation for normal spermatogenesis. Here we address the regulatory mechanisms governing cell deaths of SSCs, e.g., apoptosis, ferroptosis, pyroptosis, and cuproptosis, including transcriptional and post-transcriptional regulation, RNA-binding proteins, and epigenetic modifications (e.g., non-coding RNAs). We systematically elucidate testicular microenvironment and signaling pathways in controlling SSC deaths, including mitochondrial signaling, death receptor signaling, PI3K/AKT/mTOR, MAPK, and WNT/β-catenin pathways. We also discuss the translational applications of targeting key pathways or remodeling the microenvironment to intervene in SSC deaths. We highlight the prospects and requirements to develop the advanced technologies, e.g., the long-term in vitro human primary SSC culture systems, single cell multi-omics, novel gene editing approaches with high safety and efficiency, and translating efficacy from basic research to clinical applications. The present review aims to provide new and overall insights into better understanding the molecular mechanisms underlying cell deaths of SSCs and the pathogenesis of non-obstructive azoospermia (NOA), which could offer novel strategies for precise treatment of male infertility.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469250","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":"Structural and biochemical characterization of a novel DinG containing an endonuclease domain.","authors":"Shen Li, Tianwen Gao, Wanshan Hao, Hang Chen, Xiaolei Hu, Rong Qi, Cheng Chen, Kaiying Cheng","doi":"10.1007/s00018-026-06346-3","DOIUrl":"10.1007/s00018-026-06346-3","url":null,"abstract":"<p><p>DinG-like proteins are members of the XPD-family SF2 helicases and are widely distributed in bacteria, yet they exhibit remarkable diversity in domain architecture and biological function. A distinct subgroup of DinG homologs harboring an N-terminal PD-(D/E)XK-type nuclease domain, designated EndoDinGs, has remained uncharacterized. Here, we report the first structural and functional characterization of this subgroup using Finegoldia magna DinG (FmaDinG) as a representative example. FmaDinG displays Mn²⁺-preferred endonuclease activity together with Mg²⁺-dependent 5'-3' unidirectional helicase activity. We determined the crystal structure of the FmaDinG-ssDNA-ADPNP complex at 2.26 Å resolution. Structural and biochemical analyses reveal a direct role of the Arch domain in DNA engagement and suggest a gating mechanism within the nuclease domain that regulates DNA entry, a feature that may be specific to the EndoDinG subgroup. Key residues required for nuclease and helicase activities were identified by site-directed mutagenesis. Together, these results support a mechanistic model in which EndoDinGs such as FmaDinG function as coordinated nuclease-helicase machines for DNA processing.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444649","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":"FADS1-mediated Efferocytosis in Tumor-Associated Macrophages Shapes an Immunosuppressive Microenvironment in Gastric Cancer.","authors":"Yingjing Zhang, Rongyuan Wei, Pengfei Su, Yonghu Xu, Tian Yu, Bowen Hou, Jianchun Yu, Fenglin Liu, Yakai Huang","doi":"10.1007/s00018-026-06314-x","DOIUrl":"10.1007/s00018-026-06314-x","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) play a central role in tumor progression and therapeutic resistance. Alterations in unsaturated fatty acids (UFAs) metabolism are known to contribute to the immunosuppressive properties of TAMs. However, the complex regulatory relationship between UFAs metabolism and TAMs during gastric cancer (GC) progression remains largely unclear. Through a comprehensive analysis of single-cell RNA sequencing and transcriptomic data, we found that the UFAs biosynthesis-related enzyme FADS1 holds prognostic significance in GC within TAMs. Clinically, a high infiltration of FADS1⁺TAMs strongly correlates with poor prognosis and immunotherapy resistance across several GC cohorts. Using in vitro co-culture systems and in vivo mouse models, our data suggest that FADS1⁺TAMs actively contribute to an immunosuppressive microenvironment, potentially driving CD8⁺T cell dysfunction. Mechanistically, our findings indicate that FADS1 mediated DHA synthesis and activated PPARγ, which subsequently promotes efferocytosis and inhibit the STING-IFN-I signaling pathway in TAMs. Notably, systemic pharmacological targeting of FADS1 exerted a significant sensitizing effect in mouse ectopic GC models, inhibiting tumor growth, enhancing CD8⁺T cells cytotoxicity, and improving the efficacy of PD-1 blockade. Overall, our study highlights FADS1⁺TAMs as a critical component of GC progression and a potential exploratory biomarker for immunotherapy responsiveness. Furthermore, pharmacological inhibition of FADS1 represents a promising combinatorial strategy for reshaping the TME and enhancing immune checkpoint blockade efficacy in preclinical settings.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454869","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":"Mesenchymal stem cell-derived exosomes alleviate post-resuscitation brain injury by inhibiting neuronal ferroptosis partly via the PRMT1/SLC7A11/GPX4 pathway.","authors":"Lulu Li, Lan Ying, Lu He, Qijiang Chen, Huijuan Yang, Jinyu Zhu, Yong Liu, Li Jiang, Licai Liang, Jiefeng Xu, Mao Zhang","doi":"10.1007/s00018-026-06344-5","DOIUrl":"10.1007/s00018-026-06344-5","url":null,"abstract":"<p><strong>Background: </strong>Post-resuscitation brain injury is the main contributor to the death and disability of cardiac arrest (CA) victims. Neuronal ferroptosis is involved in the pathogenesis of brain injury after resuscitation, which becomes an effective therapeutic target. Recent studies demonstrated that mesenchymal stem cell-derived exosomes (MSC-Exo) were a promising approach for the alleviation of regional cerebral ischemia reperfusion injury; however, its effectiveness in post-resuscitation brain injury remains to be investigated. In this study, we investigated whether MSC-Exo could alleviate post-resuscitation brain injury by inhibiting neuronal ferroptosis and its regulatory mechanism.</p><p><strong>Methods and results: </strong>In vivo, a clinically relevant swine model of CA and resuscitation was established. In parallel, SH-SY5Y neuronal cells exposed to hypoxia/reoxygenation (H/R) were used as the in vitro model. We found that MSC-Exo administration provided potent protection of neuronal cells against H/R injury in vitro, and effectively alleviated brain injury after CA and resuscitation in vivo. Furthermore, we showed that the protective effects of MSC-Exo administration were associated with the upregulation of protein arginine methyltransferase 1 (PRMT1), solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) expression, and subsequent inhibition of neuronal ferroptosis in in vitro and in vivo studies. Mechanistically, MSC-Exo administration promoted the recovery of PRMT1 expression, and then the latter bound to the promoter of SLC7A11 and enhanced its transcriptional activity after H/R injury in neuronal cells. Additionally, the miR-320a-3p/tripartite motif-containing 21 (TRIM21) axis was a possible mechanism by which MSC-Exo administration activated the PRMT1/SLC7A11/GPX4 pathway in vitro.</p><p><strong>Conclusions: </strong>MSC-Exo administration effectively alleviated post-resuscitation brain injury after CA and resuscitation, which was related to the inhibition of neuronal ferroptosis partly through the activation of PRMT1/SLC7A11/GPX4 pathway.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444601","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":"Moesin is an α_νβ₃ integrin-interacting protein that affects endothelial cell activation and angiogenesis through balancing c-Met and VEGFR2 activation.","authors":"Michaela-Karina Enake, Wanjing Lai, Sotiria Tsirmoula, Κonstantinos Papadimatos, Marina Κoutsioumpa, Lamprini Skondra, Spyros Skandalis, Constantinos M Mikelis, Lingling Shi, Evangelia Papadimitriou","doi":"10.1007/s00018-026-06352-5","DOIUrl":"10.1007/s00018-026-06352-5","url":null,"abstract":"<p><p>Moesin (Msn) is a member of the ERM (Ezrin, Radixin, and Moesin) protein family implicated in cell-cell recognition, cell adhesion, and migration. In this work, we identified Msn as an α_νβ₃ integrin-interacting molecule in human endothelial cells, with a role in endothelial cell signaling and angiogenesis. Msn and its active phosphorylated form are highly expressed in endothelial cells in vitro and in vivo. Pleiotrophin and vascular endothelial growth factor A₁₆₅ (VEGFA₁₆₅), increase Msn phosphorylation and decrease the interaction of Msn with α_νβ₃ integrin. Downregulation of Msn expression in endothelial cells using siRNA reduced VEGF receptor 2 (VEGFR2) expression and activation. It also decreased permeability, collective cell migration, and tube formation in vitro, concomitant with reduced angiogenesis and blood-brain barrier permeability in Msn knockout mice. Concurrently, it decreased β₃ integrin expression, increased the c-Src- and phosphoinositide 3-kinase (PI3K)-dependent cell-surface localization of nucleolin, and activated ERK1/2 kinases and cMet. Pharmacological inhibitors of c-Src, PI3K, cell-surface nucleolin, ERK1/2, and cMet, but not of VEGFR2 or α_vβ₃ integrin, abolished siMsn-induced individual-cell motility. Taken together, these findings identify a novel binding partner of the α_vβ₃ integrin that regulates the activation of cMet and VEGFR2 in endothelial cells, clarifying the mechanisms underlying the activation of multiple angiogenic pathways and highlighting potential new targets for improving anti-angiogenic therapies.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454889","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":"LAMP2A-dependent chaperone mediated autophagy regulates Notch signaling and controls neural stem cell differentiation.","authors":"Daphne Antoniou, Maria Xilouri, Dimitrios Gkikas, Dimitrios Vlachakis, Matina Tsampoula, Nikos Malissovas, Konstantina Mastori, Valeria Kaltezioti, Elpinickie Ninou, Christina Kyrousi, Stavros Taraviras, Leonidas Stefanis, Panagiotis K Politis","doi":"10.1007/s00018-026-06330-x","DOIUrl":"10.1007/s00018-026-06330-x","url":null,"abstract":"<p><p>Protein degradation systems have profound effects on signaling pathways and molecular networks that regulate organogenesis. Chaperone Mediated Autophagy (CMA) has been linked to neurodegenerative and neurodevelopmental diseases, however, its role in mammalian brain development remains poorly understood. Here, we identify a regulatory role of CMA pathway in neural stem cell (NSC) differentiation. We show that CMA is active in NSCs, while expression of LAMP2A, the principal limiting component of CMA, is associated with the induction of neurogenesis. Most importantly, overexpression and loss-of-function experiments of LAMP2A in NSCs suggest an inductive role of CMA in neuronal differentiation. Moreover, we demonstrate that LAMP2A is involved in NSC fate decisions by interfering with NOTCH1 signaling pathway. Our data support a model in which LAMP2A-dependent CMA contributes to neuronal fate acquisition through suppression of NOTCH1 signaling, and provide a mechanistic framework that may help explain the reported genetic involvement of LAMP2 gene and CMA in neurodevelopmental disorders.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435359","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}