Cell Biology and Toxicology最新文献

{"title":"Transcriptomic changes in oxidative stress, immunity, and cancer pathways caused by cannabis vapor on alveolar epithelial cells.","authors":"Emily T Wilson, Percival Graham, David H Eidelman, Carolyn J Baglole","doi":"10.1007/s10565-025-09997-3","DOIUrl":"10.1007/s10565-025-09997-3","url":null,"abstract":"<p><p>As legalization of cannabis increases worldwide, vaping cannabis is gaining popularity due to the belief that it is less harmful than smoking cannabis. However, the safety of cannabis vaping remains untested. To address this, we developed a physiologically relevant method for in vitro assessment of cannabis vapor on alveolar epithelial cell cultures. We compared the transcriptional response in three in vitro models of cannabis vapor exposure using A549 epithelial cells in submerged culture, pseudo-air liquid interface (ALI) culture, and ALI culture coupled with the expoCube™ advanced exposure system. Baseline gene expression in ALI-maintained A549 cells showed higher expression of type 2 alveolar epithelial (AEC2) genes related to surfactant production, ion movement, and barrier integrity. Acute exposure to cannabis vapor significantly affected gene expression in AEC2 cells belonging to pathways related to cancer, oxidative stress, and the immune response without being associated with a DNA damage response. This study identifies potential risks of cannabis vaping and underscores the need for further exploration into its respiratory health implications.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"57"},"PeriodicalIF":5.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Andrographolide ameliorates sepsis-induced acute liver injury by attenuating endoplasmic reticulum stress through the FKBP1A-mediated NOTCH1/AK2 pathway.","authors":"Jiaqi He, Zepeng Huang, Rui Zou","doi":"10.1007/s10565-025-10007-9","DOIUrl":"10.1007/s10565-025-10007-9","url":null,"abstract":"<p><p>Andrographolide (AP) has been shown to possess anti-inflammatory activities. In this study, the impact of AP in sepsis-induced acute liver injury (ALI) and the molecules involved were dissected. FKBP1A was predicted to be the sole target protein of AP that was also differentially expressed in the GSE166868 dataset. AP induced the protein expression of FKBP1A and suppressed that of NOTCH1 in a dose-dependent manner. AP ameliorated ALI in mice induced by D-galactosamine and LPS and inhibited LPS-induced liver parenchymal cell injury in vitro. By contrast, the protective effect of AP was significantly lost after the knockdown of FKBP1A. As a positive control, the therapeutic effect of dexamethasone on ALI may be related to NOTCH1, which was not related to FKBP1A. NOTCH1 promoted AK2 transcription in liver parenchymal cells, and FKBP1A inhibited endoplasmic reticulum (ER) stress by impairing NOTCH1/AK2 signaling. Restoration of NOTCH1 significantly reversed the hepatoprotective effect of AP in ALI mice and LPS-induced liver parenchymal cell injury by activating the ER stress pathway. Therefore, AP-promoted FKBP1A expression inhibits ALI progression by blocking the NOTCH1/AK2-mediated ER pathway.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"56"},"PeriodicalIF":5.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The microRNA-mediated apoptotic signaling axis in male reproduction: a possible and targetable culprit in male infertility.","authors":"Pengxia Yu, Xue Zhao, Dan Zhou, Songtao Wang, Zihuan Hu, Kai Lian, Nanhui Zhang, Peng Duan","doi":"10.1007/s10565-025-10006-w","DOIUrl":"10.1007/s10565-025-10006-w","url":null,"abstract":"<p><p>Recently, infertility has emerged as a significant and prevalent public health concern warranting considerable attention. Apoptosis, recognized as programmed cell death, constitutes a crucial process essential for the maintenance of normal spermatogenesis. Multiple investigations have illustrated that the dysregulated apoptosis of reproductive cells, encompassing spermatogonial stem cells, Sertoli cells, and Leydig cells, serves as a causative factor in male infertility. MicroRNAs represent a class of small RNA molecules that exert negative regulatory control over gene expression using direct interaction with messenger RNA transcripts. Previous studies have established that aberrant expression of miRNAs induces apoptosis in reproductive tissues, correlating with reproductive dysfunctions and infertility. In this review, we offer a comprehensive overview of miRNAs and their respective target genes implicated in the apoptotic process. As well, miRNAs are involved in multiple apoptotic signaling pathways, namely the PI3K/AKT, NOTCH, Wnt/β-catenin, and mTOR signaling cascades, exerting both negative and positive effects. We additionally elucidate the significant functions played by lncRNAs and circular RNAs as competing endogenous RNAs in the process of apoptosis within reproductive cells. We further illustrate that external factors, including silica nanoparticles, Cyclosporine A, and smoking, induce dysregulation of miRNAs, resulting in apoptosis within reproductive cells and subsequent male reproductive toxicity. Further, we discuss the implication of heat stress, hypoxia, and diabetes in reproductive cell apoptosis induced by miRNA dysregulation in male infertility. Finally, we demonstrate that the modulation of miRNAs via traditional and novel medicine could protect reproductive cells from apoptosis and be implemented as a therapeutic approach in male infertility.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"54"},"PeriodicalIF":5.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil-derived heparin-binding protein increases endothelial permeability in acute lung injury by promoting TRIM21 and the ubiquitination of P65.","authors":"Jian Zhang, Yong Cao, Wenqi Shu, Senxiao Dong, Yini Sun, Xiaochun Ma","doi":"10.1007/s10565-025-10005-x","DOIUrl":"10.1007/s10565-025-10005-x","url":null,"abstract":"<p><p>Acute lung injury (ALI), which poses a significant public health threat, is commonly caused by sepsis. ALI is associated with permeability and glycolysis changes in pulmonary microvascular endothelial cells. Our study demonstrates that heparin-binding protein (HBP), released from neutrophils during sepsis, exacerbates endothelial permeability and glycolysis, thereby triggering ALI. Through coimmunoprecipitation and mass spectrometry, TRIM21 was identified as a HBP interaction partner. Notably, HBP enhances the protein stability of TRIM21 by inhibiting K48 ubiquitination. TRIM21 binds to and promotes K63-linked ubiquitination of P65, facilitating its nuclear translocation. TRIM21 regulates HPMEC permeability and glycolysis in a manner dependent on P65 nuclear translocation. HBP stabilizes TRIM21 and enhances TRIM21 interactions with P65. Rescue experiments conducted in vivo and in vitro demonstrate that modulation of endothelial permeability and glycolysis by HBP is predominantly mediated through the TRIM21-P65 axis. Our results suggest that targeting the HBP/TRIM21/P65 axis is a novel therapeutic strategy to ameliorate ALI.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"55"},"PeriodicalIF":5.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycolysis regulates palatal mesenchyme proliferation through Pten-Glut1 axis via Pten classical and non-classical pathways.","authors":"Yijia Wang, Xia Peng, Xiaotong Wang, Jing Chen, Xiaoyu Zheng, Xige Zhao, Cui Guo, Juan Du","doi":"10.1007/s10565-025-10000-2","DOIUrl":"10.1007/s10565-025-10000-2","url":null,"abstract":"<p><p>Abnormal embryonic development leads to the formation of cleft palate (CP) which is difficult to be detected by genetic screening and needs sequent treatment from infants to adults. There are no interceptive treatment about CP until now. Germline deletion of phosphatase and tensin homolog (Pten) was related to embryonic malformation and regulated tumor cell proliferation through glycolysis. However, the role of Pten in CP and the relationship between CP, Pten, and glycolysis are unknown. In our research, we constructed Pten knockdown models in vitro and in vivo. Our results provided preliminary evidence that blocking Pten by its inhibitor such as VO-OHpic might be an effective interceptive treatment in early period of palate development when pregnant mother expose in harmful environment during the early period of palate development to reducing CP occurring which was related with the crosstalk between Pten, and glycolysis in the process.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"53"},"PeriodicalIF":5.3,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanism of ZC3H13 -mediated ferroptosis in doxorubicin resistance of triple negative breast cancer.","authors":"Li Huang, Lei Han, Shuai Liang, Guohui Han","doi":"10.1007/s10565-024-09980-4","DOIUrl":"10.1007/s10565-024-09980-4","url":null,"abstract":"<p><strong>Background: </strong>Triple negative breast cancer (TNBC) continues to be the most aggressive subtype of breast cancer that frequently develops resistance to chemotherapy. Doxorubicin (DOX) belongs to the anthracycline chemical class of the drug and is one of the widely used anticancer drugs. This study investigates the mechanism of m6A methyltransferase ZC3H13 in DOX resistance of TNBC.</p><p><strong>Methods: </strong>ZC3H13, KCNQ1OT1, and TRABD expressions in TNBC tissues or cells were detected by RT-qPCR or Western blot. The effect of ZC3H13 on DOX resistance of TNBC cells was evaluated by CCK-8, clone formation, and EdU staining. RIP was performed to analyze the enrichment of YTHDF2 or m6A on KCNQ1OT1. RIP and RNA pull-down verified the binding between KCNQ1OT1 and MLL4. The enrichment of MLL or H3K9me1/2/3 on TRABD promoter was analyzed by ChIP. A nude mouse xenograft tumor model was established to verify the mechanism in vivo.</p><p><strong>Results: </strong>ZC3H13 was poorly expressed in TNBC, and its expression further decreased in drug-resistant cells. Overexpression of ZC3H13 decreased the IC50 of drug-resistant TNBC cells to DOX, repressed proliferation, and induced ferroptosis. Mechanistically, ZC3H13-mediated m6A modification reduced the transcriptional stability of KCNQ1OT1 and inhibited its expression in a YTHDF2-dependent manner. KCNQ1OT1 enhanced the enrichment of H3K4me1/2/3 on TRABD promoter by recruiting MLL4, thus increasing TRABD expression. ZC3H13 induced ferroptosis by inhibiting KCNQ1OT1/TRABD, thereby restraining the growth of DOX-treated tumors in vivo.</p><p><strong>Conclusion: </strong>ZC3H13-mediated m6A modification reduces DOX resistance in TNBC by promoting ferroptosis via KCNQ1OT1/TRABD axis.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"52"},"PeriodicalIF":5.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11861033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143498998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic role of hucMSC-sEV-enriched miR-13896 in cisplatin-induced acute kidney injury through M2 macrophage polarization.","authors":"Can Jin, Peipei Wu, Wei Wu, Wenya Chen, Wanzhu Liu, Yuan Zhu, QiShun Wu, Binghai Chen, Cheng Ji, Hui Qian","doi":"10.1007/s10565-025-09998-2","DOIUrl":"10.1007/s10565-025-09998-2","url":null,"abstract":"<p><p>Human umbilical cord mesenchymal stem cell-derived small extracellular vesicles (hucMSC-sEV) have recently garnered attention as a potential therapeutic approach for kidney diseases with anti-inflammatory effects. Infiltrated macrophages play an important role in facilitating tissue regeneration. However, the intricate regulatory effects of hucMSC-sEV on macrophages during cisplatin-induced acute kidney injury (AKI) remain unknown. In this study, we uncovered that hucMSC-sEV exhibited potent anti-inflammation and effectively inhibited the polarization of M1 phenotype macrophages. Mechanically, miRNA sequencing analysis and qRT-PCR indicated that a novel miRNA, named miR-13896, was enriched in hucMSC-sEV. When transfected with miR-13896 mimic, macrophages displayed M2 phenotype with elevated levels of Arg1 and IL-10, while miR-13896 inhibitor promoted M1 phenotype. Furthermore, we firstly established that miR-13896 repressed Tradd expression by targeting its 3' untranslated region and subsequently inhibited NF-κB signaling pathway in macrophages. Additionally, to improve therapeutic effects, hucMSC-sEV were engineered with elevated levels of miR-13896 through electroporation, which resulted in promoting M2 phenotype macrophages, inhibiting inflammatory factors, and enhancing kidney repair. Conclusively, our findings provide novel insights into the mechanisms underlying the effects of hucMSC-sEV on macrophages and AKI, while also highlighting electroporation as a promising strategy for treating cisplatin-induced AKI.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"50"},"PeriodicalIF":5.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MCM8 promotes NR4A1-mediated E2F1 transcription and facilitates renal cell carcinoma through enhancing aerobic glycolysis.","authors":"Shaobo Zhang, Haoqi Miao, Tian Han, Xiangzhen Wu, Chao Liang, Jian Qian, Pengfei Shao","doi":"10.1007/s10565-025-10002-0","DOIUrl":"10.1007/s10565-025-10002-0","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC) is a type of renal malignancy originated from the urinary tubular epithelial system. Despite its high incidence, the molecular mechanisms driving its pathogenesis remain poorly understood, limiting therapeutic advancements. This study explored the link between MCM8 and RCC progression. MCM8 displays significantly high expression in RCC tissues and was closely associated with RCC pathological staging. Knocking down endogenous MCM8 in RCC cells significantly suppressed malignant phenotypes, while simultaneously inducing apoptosis. Similarly, in vivo experiments confirmed these findings, showing a pronounced reduction in tumor growth upon MCM8 silencing. Mechanistic investigations revealed that MCM8 regulates E2F1 expression by interacting with the transcription factor NR4A1, thereby affecting E2F1 transcriptional activity. Additionally, MCM8 and E2F1 collaboratively influence aerobic glycolysis and the cellular behavior of RCC cells. In conclusion, this study identifies MCM8 as a tumor-promoting factor in RCC, with its oncogenic role potentially mediated by its regulation of E2F1 expression.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"51"},"PeriodicalIF":5.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatio-temporal transcriptomic analysis reveals distinct nephrotoxicity, DNA damage, and regeneration response after cisplatin.","authors":"Lukas S Wijaya, Steven J Kunnen, Panuwat Trairatphisan, Ciarán P Fisher, Meredith E Crosby, Kai Schaefer, Karen Bodié, Erin E Vaughan, Laura Breidenbach, Thomas Reich, Diana Clausznitzer, Sylvestre Bonnet, Sipeng Zheng, Chantal Pont, James L Stevens, Sylvia E Le Dévédec, Bob van de Water","doi":"10.1007/s10565-025-10003-z","DOIUrl":"10.1007/s10565-025-10003-z","url":null,"abstract":"<p><p>Nephrotoxicity caused by drug or chemical exposure involves complex mechanisms as well as a temporal integration of injury and repair responses in different nephron segments. Distinct cellular transcriptional programs regulate the time-dependent tissue injury and regeneration responses. Whole kidney transcriptome analysis cannot dissect the complex spatio-temporal injury and regeneration responses in the different nephron segments. Here, we used laser capture microdissection of formalin-fixed paraffin embedded sections followed by whole genome targeted RNA-sequencing-TempO-Seq and co-expression gene-network (module) analysis to determine the spatial-temporal responses in rat kidney glomeruli (GM), cortical proximal tubules (CPT) and outer-medulla proximal tubules (OMPT) comparison with whole kidney, after a single dose of the nephrotoxicant cisplatin. We demonstrate that cisplatin induced early onset of DNA damage in both CPT and OMPT, but not GM. Sustained DNA damage response was strongest in OMPT coinciding with OMPT specific inflammatory signaling, actin cytoskeletal remodeling and increased glycolytic metabolism with suppression of mitochondrial activity. Later responses reflected regeneration-related cell cycle pathway activation and ribosomal biogenesis in the injured OMPT regions. Activation of modules containing kidney injury biomarkers was strongest in OMPT, with OMPT Clu expression highly correlating with urinary clusterin biomarker measurements compared the correlation of Kim1. Our findings also showed that whole kidney responses were less sensitive than OMPT. In conclusion, our LCM-TempO-Seq method reveals a detailed spatial mechanistic understanding of renal injury/regeneration after nephrotoxicant exposure and identifies the most representative mechanism-based nephron segment specific renal injury biomarkers.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"49"},"PeriodicalIF":5.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11845422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired olfactory bulb neurogenesis mediated by Notch1 contributes to olfactory dysfunction in mice chronically exposed to methamphetamine.","authors":"Cihang Gu, Zhuo Wang, Wenyu Luo, Haosen Ling, Xilie Cui, Tongtong Deng, Kuan Li, Wei Huang, Qiqian Xie, Bowen Tao, Xiaolan Qi, Xiaojia Peng, Jiuyang Ding, Pingming Qiu","doi":"10.1007/s10565-025-10004-y","DOIUrl":"10.1007/s10565-025-10004-y","url":null,"abstract":"<p><p>Methamphetamine (Meth) is a potent central nervous system stimulant with high addictive potential and neurotoxic effects. Chronic use results in significant damage in various brain functions, including cognition, memory, and sensory perception. Olfactory dysfunction is a notable yet often overlooked consequence of Meth abuse, and its underlying mechanisms are not fully understood. This study investigates the mechanisms of Meth-induced olfactory impairment through a thorough examination of olfactory bulb (OB) neurogenesis. We found that chronic Meth abuse impaired olfactory function in mice by not only reducing the self-renewal of subventricular zone (SVZ) neural stem cells (NSCs) but also altering their differentiation potential, leading their differentiation into astrocytes at the expense of neurons. Mechanistically, Meth inhibits autophagosome-lysosome fusion by downregulating Syntaxin 17 (Stx17), which reduces autophagic flux. In NSCs, autophagy tightly regulates Notch1 levels, and impaired autophagic degradation of Notch1 leads to its abnormal activation. This alters NSCs fate determination, ultimately affecting OB neurogenesis. Our study reveals that Meth impairs olfactory function through autophagic dysfunction and aberrant Notch1 signaling. Understanding these mechanisms not only provides new insights into Meth-induced olfactory dysfunction but also offers potential targets for developing therapies to alleviate Meth-induced neurotoxicity and sensory damage in the future.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"46"},"PeriodicalIF":5.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}