Cellular and Molecular Life Sciences最新文献

{"title":"SETD2 drives METTL14-mediated m⁶A to suppress Piezo1 Attenuation and activate TGM2 to promote pulmonary hypertension.","authors":"Shuai-Shuai Zhao, Chuan Yuan, Jin-Long Liu, Qi-Cai Wu, Xue-Liang Zhou","doi":"10.1007/s00018-025-05809-3","DOIUrl":"10.1007/s00018-025-05809-3","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary arterial hypertension (PAH) is characterized by pathological vascular remodeling driven by pulmonary artery smooth muscle cell (PASMC) proliferation. While METTL14-mediated N6-methyladenosine (m⁶A) RNA modification has been implicated in PAH, the upstream regulators and downstream effectors linking m⁶A to PASMC dysregulation remain unclear. This study investigates the role of SETD2, a histone methyltransferase, in driving METTL14-dependent m⁶A modifications to promote PAH via Piezo1 and transglutaminase 2 (TGM2).</p><p><strong>Methods: </strong>C57BL/6 mice were subjected to hypoxia, and pulmonary artery smooth muscle cells (PASMCs) were periodically stretched to establish PAH models in vivo and in vitro. The epigenetic regulation of METTL14 by SETD2-mediated H3K36me3 was investigated by chromatin immunoprecipitation (ChIP). Methylated RNA immunoprecipitation sequence (MeRIP-seq), RNA-seq, and dual-luciferase reporter gene data were used to determine whether METTL14 enhances the expression of Piezo1 in an m⁶A-dependent manner. To analyze comparisons between multiple datasets, one-way ANOVA was used.</p><p><strong>Results: </strong>METTL14 overexpression increased PASMC proliferation by 1.45-fold (vs. controls) and elevated global m⁶A levels by 1.73-fold in total RNA and 1.43-fold in poly A + RNA. SETD2-driven H3K36me3 histone modification upregulated METTL14 expression by 1.76-fold, amplifying m⁶A deposition. In hypoxia-induced PAH mice, METTL14 overexpression exacerbated hemodynamic severity, increasing right ventricular systolic pressure (RVSP) by 29% and mean pulmonary arterial pressure (mPAP) by 33% (vs. hypoxia alone). SETD2 knockout in PASMCs reduced RVSP by 24%, mPAP by 28%, and pulmonary artery media thickness (PAMT) by 29%, while decreasing m⁶A levels by 48%. Piezo1 mRNA stability increased by 2.36-fold via METTL14-mediated m⁶A modification at adenosine 1080, elevating Piezo1 protein expression by 3.58-fold in PASMCs. Piezo1 overexpression increased intracellular Ca²⁺ influx, driving TGM2 activity by 1.79-fold and restoring PASMC proliferation despite SETD2 deficiency.</p><p><strong>Conclusions: </strong>This study identifies a novel SETD2/H3K36me3/METTL14/m⁶A axis that stabilizes Piezo1 mRNA, promoting Ca²⁺-dependent TGM2 activation and PASMC proliferation in PAH. Targeting this pathway-via SETD2, METTL14, or Piezo1 inhibition-may offer therapeutic potential to ameliorate vascular remodeling in PAH.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"302"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798285","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":"Inhibition of STING-induced mitochondrial Drp1/N-GSDMD-mediated MtDNA release alleviates Sepsis-induced lung injury.","authors":"Shishi Zou, Yifan Zuo, Yukai Chen, Tianyu Zhang, Tinglv Fu, Guorui Li, Rui Xiong, Bohao Liu, Yong Hu, Zhaoyu Hu, Chunguang Miao, Xiaojing Wu, Ning Li, Qing Geng","doi":"10.1007/s00018-025-05774-x","DOIUrl":"10.1007/s00018-025-05774-x","url":null,"abstract":"<p><p>The stimulator of interferon genes (STING) pathway serves as a crucial nexus in inflammatory responses and cell death. Despite its role in Mitochondria-Endoplasmic Reticulum Contact (MERC), the mechanistic contributions to inflammatory outcomes remain poorly understood. In clinical acute respiratory distress syndrome (ARDS) models of COVID-19 infection and animal models of LPS-induced acute lung injury (ALI), the STING pathway is closely associated with the pyroptosis pathway. The macrophage STING-N-GSDMD-mtDNA positive feedback loop, upon LPS challenge, induces inflammatory responses and pyroptosis. The GSDMD inhibitor disulfiram (DSF) specifically abrogates the N-terminal portion of GSDMD anchored to the mitochondrial membrane. Furthermore, macrophage STING mediates the direct interaction between Drp1 and N-GSDMD on mitochondrial membrane by regulating mitochondrial calcium, linking mitochondrial fission to the induction of inflammatory responses. Targeting STING-mediated mitochondrial homeostasis, both genetically and pharmacologically, may play a protective role in preventing and treating sepsis-induced acute lung injury. Overall, our study posits that STING deficiency mitigates the cooperative interaction between N-GSDMD and Drp1 in mediating mitochondrial permeabilization and rupture following LPS challenge, paving the way for further investigations into inflammation and pyroptosis.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"305"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798281","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":"Regulation and dysregulation of microRNA - transcription factor axes in differentiation and neuroblastoma.","authors":"Fakhira H Nazki, Cameron P Bracken","doi":"10.1007/s00018-025-05832-4","DOIUrl":"10.1007/s00018-025-05832-4","url":null,"abstract":"<p><p>Development is characterized by dynamic changes in gene expression as cells traverse genetic pathways and make lineage-specific commitments. Transcription factors, which drive gene expression, and microRNAs, the largest class of post-transcriptional regulators, often function together within the same genetic networks. These interactions frequently include direct regulation of one another and shared target genes, forming feedback and feedforward loops that fine-tune gene expression to establish and maintain cell identity. The interplay between transcriptional and post-transcriptional regulation is particularly extensive during development, where disruptions in gene expression programs can cause cells to become trapped in immature proliferative states that result in paediatric cancers. This review focuses on the intricate cross-regulation between transcription factors and microRNAs, highlighting their contributions to developmental cancers with a particular emphasis on neuroblastoma, the most prevalent extracranial solid tumour in children, which arises from the failure of neural crest-derived cells to properly differentiate during sympathoadrenal development.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"304"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798283","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":"Spider venom peptides with unique fold selectively block Shaker-type potassium channels.","authors":"Alexey I Kuzmenkov, Valentina A Iunusova, Vladislav A Lushpa, Yakov A Deyev, Vladislav V Babenko, Daniil V Osipov, Antonina A Berkut, Jan Tytgat, Eduard V Bocharov, David J Adams, Rocio K Finol-Urdaneta, Alexander A Vassilevski","doi":"10.1007/s00018-025-05778-7","DOIUrl":"10.1007/s00018-025-05778-7","url":null,"abstract":"<p><p>Natural toxins are highly effective at targeting ion channels with high selectivity and potency. To date, all identified spider venom peptide toxins that modulate voltage-gated potassium (K_V) channels inhibit Shab (K_V2) or Shal-related isoforms (K_V4) by interacting with their voltage-sensing domains. In this study, we report novel spider-derived pore-blocking toxins that selectively target Shaker-type (K_V1) channels with nanomolar potency. We isolated murinotoxins MnTx-1 and MnTx-2 from the orange baboon tarantula Pterinochilus murinus and sequenced them using a combination of Edman degradation, mass spectrometry, and venom gland nanopore transcriptomics. MnTx-1 was produced recombinantly, and its NMR solution structure was determined. Although MnTx-1 shares sequence motifs common to spider toxins, it displays a distinctly different three-dimensional structure, featuring an alternative disulfide linkage, which we have termed the Disulfide-Reined Hairpin (DRH). We attribute the unique pharmacology of MnTx-1 to its unusual spatial structure. The DRH motif represents a promising new miniature scaffold for future bioengineering applications.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"300"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798286","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 complex web of membrane contact sites in brain aging and neurodegeneration.","authors":"Domenico Azarnia Tehran, Paola Pizzo","doi":"10.1007/s00018-025-05830-6","DOIUrl":"10.1007/s00018-025-05830-6","url":null,"abstract":"<p><p>To sustain the essential biological functions required for life, eukaryotic cells rely on complex interactions between different intracellular compartments. Membrane contact sites (MCS), regions where organelles come into close proximity, have recently emerged as major hubs for cellular communication, mediating a broad range of physiological processes, including calcium signalling, lipid synthesis and bioenergetics. MCS are particularly abundant and indispensable in polarized and long-lived cells, such as neurons, where they support both structural and functional integrity. In this review, we explore the functional diversity, molecular composition, and dynamic regulation of key mammalian MCS: endoplasmic reticulum (ER)-plasma membrane, ER-mitochondria and contact sites involving lipid droplets. We highlight their central role in neuronal health and discuss how MCS dysfunction has increasingly been recognized as a hallmark of brain aging and various neurodegenerative diseases, most notably Alzheimer's disease, where altered MCS dynamics contribute to pathogenesis. Finally, we emphasize the therapeutic potential of targeting MCS and outline key unanswered questions to guide future research.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"301"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798287","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":"RNA modification is the mark and strategy for host-microbe interactions.","authors":"Ye Tian, Xiaoyun Wang","doi":"10.1007/s00018-025-05842-2","DOIUrl":"10.1007/s00018-025-05842-2","url":null,"abstract":"<p><p>Pathogenic microbes need to adapt to host environments during infection. With advances in sequencing technologies, RNA modifications have been shown to play a pivotal role in pathogen adaptability on a global scale. In this review, we highlight recent advances in RNA modifications that are utilized as the strategy for pathogens to survive in the host. Specifically, we summarize the studies of RNA modifications in the pathogenic bacteria, fungi, viruses, parasites, and host. We also discuss the anti-infection potential of targeting RNA modifications.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"306"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798284","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":"DNA glycosylases Ogg1 and Mutyh influence gene expression of PRC2 targets associated with cognition.","authors":"Andreas Abentung, Teri Sakshaug, Rabina Dumaru, Nina-Beate Liabakk, Mingyi Yang, Junbai Wang, Magnar Bjørås, Katja Scheffler","doi":"10.1007/s00018-025-05730-9","DOIUrl":"10.1007/s00018-025-05730-9","url":null,"abstract":"<p><p>Base excision repair, initiated by DNA glycosylases, preserves genomic integrity by removing damaged bases. DNA glycosylases Ogg1 and Mutyh were shown to alter the hippocampal transcriptome independently of DNA damage repair. However, the role of DNA glycosylases as transcriptional regulators and their involvement in cognition remain unclear. Here, we combine transcriptomic and epigenomic analyses of the hippocampus in mice deficient in DNA glycosylases. We report that the combined deficiency of Ogg1 and Mutyh impairs spatial long-term memory. Mechanistically, Ogg1 and Mutyh modulate DNA methylation of polycomb repressive complex 2 (PRC2) target genes. PRC2 occupancy and associated histone post-translational modifications depend on Ogg1 and Mutyh in neurons and glia. These epigenetic changes correlate with cell-type specific differences in gene expression of PRC2 targets. Finally, human genetic data link DNA glycosylase-regulated genes to cognitive function, highlighting a novel role for Ogg1 and Mutyh in modulating the epigenome to control transcriptional responses relevant for brain-related diseases.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"307"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798280","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":"Signalling pathways and cellular functions of KDEL receptors: implications in cancer biology.","authors":"Beatrice Dufrusine, Ilaria Cela, Chiara Gramegna Tota, Marta Palumbo, Michele Sallese","doi":"10.1007/s00018-025-05820-8","DOIUrl":"10.1007/s00018-025-05820-8","url":null,"abstract":"<p><p>KDEL receptors (KDELRs) are a small family of seven-transmembrane domain proteins primarily localized to the membranes of the Golgi apparatus and endoplasmic reticulum (ER). These receptors are responsible for retrieving ER-resident chaperones that have trafficked to post-ER compartments. Beyond their primary role in retrieval, chaperone binding to KDELRs trigger diverse signalling pathways. These include the activation of protein kinase A, Src tyrosine kinase, and Rab1a/Rab3a that are mediated respectively by the α-subunits Gαs, Gαq, and Gαo of heterotrimeric G-proteins. KDELR-activated signalling pathways regulate intracellular transport of proteins and membranes, extracellular matrix (ECM) degradation, and the formation of membrane protrusions from the plasma membranes. More recently, crosstalk with the EGF receptor has been reported, offering a potential explanation for how chaperones, often overrepresented on the plasma membrane of cancer cells, may contribute to enhanced cell proliferation. Reflecting their established cellular roles, numerous studies have documented significant involvement of these receptors in a broad spectrum of cancers including colorectal cancer, breast tumours, glioblastoma, melanoma, chondrosarcoma, and lung adenocarcinoma. The strong association between KDELRs and cancer is further highlighted by the observed correlation between KDELR expression and immune cell infiltration in tumours. This effect may arise from the influence of KDELRs on the secretory pathway, alongside the immunomodulatory role of KDELR1 within immune cells. In conclusion, endomembrane-initiated signalling through KDELR plays a pivotal role in regulating fundamental cellular processes, maintaining physiological functions, and modulating key aspects of cancer biology.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"299"},"PeriodicalIF":6.2,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12328878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788384","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":"Blocking NKG2A in Echinococcus multilocularis infection partially relieves impairment of NK cell function of the host.","authors":"Ayinuer Aierken, Aili Aierken, Kalibixiati Aimulajiang, Abuduaini Abulizi, Zhongdian Yuan, Chang Liu, Dalong Zhu, Hanyue Zhao, Tuerganaili Aji","doi":"10.1007/s00018-025-05838-y","DOIUrl":"10.1007/s00018-025-05838-y","url":null,"abstract":"<p><strong>Background: </strong>Alveolar echinococcosis (AE) is a fatal zoonotic parasitic disease with biological characteristics similar to cancer. Although previous studies have reported immune dysfunction of Natural Killer (NK) cells due to other inhibitory receptors in AE, limited research has been conducted on the role of Natural Killer cell protein Group 2-A (NKG2A) in human NK cells.</p><p><strong>Methods and results: </strong>Our study revealed upregulation of NKG2A expression in peripheral blood and liver tissue NK cells in patients with AE, which was accompanied by a decrease in the secretion of IFN-γ, TNF-α, and Granzyme B by these NK cells. When we blocked the NKG2A receptor during co-culture of NK cells with Echinococcus multilocularis (E. multilocularis) proteins in vitro, we observed increased secretion of IFN-γ, TNF-α, and Granzyme B by NK cells. This observation was further confirmed in an E. multilocularis-infected mice model, in which higher expression levels of NKG2A on NK cells were detected, accompanied by a reduction in IFN-γ, TNF-α and Granzyme B secretion from NK cells. Deletion of NK cells in an E. multilocularis-infected mice model clearly resulted in more aggressive disease progression. Conversely, blocking NKG2A on NK cells results in increased secretion of TNF-α, and Granzyme B by NK cells. Similar changes in NKG2A expression and NK cell quality were observed in a mice model of splenic NK cells, as well as the functional recovery of NK cells after blocking NKG2A.</p><p><strong>Conclusion: </strong>Our results demonstrate the involvement of NKG2A in impaired NK cell function during E. multilocularis infection in both humans and mice, suggesting that targeting NKG2A through blockade has the potential to restore NK cell function against this infection.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"297"},"PeriodicalIF":6.2,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12317963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768467","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":"Disruption of hnRNP A2-mediated RNA dynamics by amyloid-β drives MBP increase in Alzheimer's disease.","authors":"Adhara Gaminde-Blasco, Rodrigo Senovilla-Ganzo, Uxue Balantzategi, Maialen Martinez-Preciado, Estibaliz Capetillo-Zarate, Fernando García-Moreno, Carlos Matute, Jimena Baleriola, Elena Alberdi","doi":"10.1007/s00018-025-05823-5","DOIUrl":"10.1007/s00018-025-05823-5","url":null,"abstract":"<p><p>Oligodendrocyte dysfunction, myelin degeneration, and white matter changes are critical events in the cognitive decline of Alzheimer's disease (AD). Amyloid-β peptide (Aβ), a hallmark of AD, disrupts oligodendrocyte and myelin homeostasis, through mechanisms that remain poorly understood. Here, transcriptomic profiling of Aβ-exposed oligodendrocytes revealed widespread gene expression changes, particularly in RNA-related processes. Among these, hnRNP A2, a key regulator of RNA transport and myelin protein regulation, was aberrantly upregulated in hippocampal oligodendrocytess from AD patients with high Aβ levels, from AD mouse models, and in Aβ-treated oligodendrocytes. RNA-immunoprecipitation sequencing of the hnRNP A2 interactome revealed Aβ-induced changes in mRNA interactions, particularly enriched binding to Mbp and Mobp, indicating impaired RNA metabolism of myelin components. Furthermore, Aβ, through hnRNP A2 disruption, increased the number, cargo and dynamics of Mbp- and Mobp-containing granules, enhanced MBP and MOBP synthesis, and decreased oligodendroglial voltage-gated Ca²⁺ influx in an MBP-dependent manner. These findings suggest that Aβ-induced dysregulation of hnRNP A2 impairs RNA metabolism and myelin protein synthesis, altering the intracellular Ca²⁺ homeostasis critical for oligodendrocyte function.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"298"},"PeriodicalIF":6.2,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12317959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768468","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}