IF 5.5 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-03-11 DOI: 10.1080/21505594.2025.2473631

Haoxiang Huang, Bohong Chen, Cong Feng, Wei Chen, Dapeng Wu

{"title":"Exploring the causal role of pathogen-derived antibodies in major urinary and kidney diseases: Insights from generalized summary data-based Mendelian randomization.","authors":"Haoxiang Huang, Bohong Chen, Cong Feng, Wei Chen, Dapeng Wu","doi":"10.1080/21505594.2025.2473631","DOIUrl":"10.1080/21505594.2025.2473631","url":null,"abstract":"Chronic kidney and urinary tract diseases, including glomerulonephritis, nephrotic syndrome, and chronic kidney disease (CKD), present significant global health challenges. Recent studies suggest a complex interplay between infectious pathogens and immune-mediated kidney damage. This study employs Generalized Summary data-based Mendelian Randomization (GSMR) to explore causal relationships between pathogen-derived antibodies and major urinary and kidney diseases.We conducted a two-sample MR analysis using summary statistics from large-scale Genome-Wide Association Studies (GWAS) to assess associations between 46 pathogen-specific antibodies and seven urinary system diseases. We utilized robust statistical methods, including inverse variance weighting, to ascertain causal effects while controlling for potential confounders.Significant associations were identified between several pathogen-specific antibodies and disease risk. Notably, Epstein-Barr virus (EBNA-1) antibody levels were inversely associated with glomerulonephritis and nephrotic syndrome, indicating a potential protective effect. Conversely, Anti-Merkel cell polyomavirus IgG seropositivity was linked to increased risks of CKD and glomerulonephritis. Additionally, immune-mediated mechanisms were highlighted, with certain antibodies exhibiting dual roles as risk factors or protective agents.This study underscores the complex role of pathogen antibodies in the pathogenesis of kidney and urinary tract diseases, revealing significant implications for future research and potential therapeutic strategies. The findings advocate for further investigation into specific pathogen interactions with the immune system, aiming to inform targeted interventions.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2473631"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143543803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactic acid in the vaginal milieu modulates the Candida-host interaction. 阴道环境中的乳酸调节念珠菌与宿主的相互作用。

IF 5.5 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-01-22 DOI: 10.1080/21505594.2025.2451165

Diletta Rosati, Marisa Valentine, Mariolina Bruno, Arnab Pradhan, Axel Dietschmann, Martin Jaeger, Ian Leaves, Frank L van de Veerdonk, Leo A B Joosten, Sumita Roy, Mark H T Stappers, Neil A R Gow, Bernhard Hube, Alistair J P Brown, Mark S Gresnigt, Mihai G Netea

{"title":"Lactic acid in the vaginal milieu modulates the Candida-host interaction.","authors":"Diletta Rosati, Marisa Valentine, Mariolina Bruno, Arnab Pradhan, Axel Dietschmann, Martin Jaeger, Ian Leaves, Frank L van de Veerdonk, Leo A B Joosten, Sumita Roy, Mark H T Stappers, Neil A R Gow, Bernhard Hube, Alistair J P Brown, Mark S Gresnigt, Mihai G Netea","doi":"10.1080/21505594.2025.2451165","DOIUrl":"10.1080/21505594.2025.2451165","url":null,"abstract":"Vulvovaginal candidiasis (VVC) is one of the most common infections caused by Candida albicans. VVC is characterized by an inadequate hyperinflammatory response and clinical symptoms associated with Candida colonization of the vaginal mucosa. Compared to other host niches in which C. albicans can cause infection, the vaginal environment is extremely rich in lactic acid that is produced by the vaginal microbiota. We examined how lactic acid abundance in the vaginal niche impacts the interaction between C. albicans and the human immune system using an in vitro culture in vaginal simulative medium (VSM). The presence of lactic acid in VSM (VSM+LA) increased C. albicans proliferation, hyphal length, and its ability to cause damage during subsequent infection of vaginal epithelial cells. The cell wall of C. albicans cells grown in VSM+LA displayed a robust mannan fibrillar structure, β-glucan exposure, and low chitin content. These cell wall changes were associated with altered immune responses and an increased ability of the fungus to induce trained immunity. Neutrophils were compromised in clearing C. albicans grown in VSM+LA conditions, despite mounting stronger oxidative responses. Collectively, we found that fungal adaptation to lactic acid in a vaginal simulative context increases its immunogenicity favouring a pro-inflammatory state. This potentially contributes to the immune response dysregulation and neutrophil recruitment observed during recurrent VVC.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2451165"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11760238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines. α -亚麻酸介导的宫颈癌细胞系表观遗传重编程。

IF 2.9 3区生物学

Epigenetics Pub Date : 2025-12-01 Epub Date: 2025-02-02 DOI: 10.1080/15592294.2025.2451551

Amrita Ulhe, Prerna Raina, Amol Chaudhary, Ruchika Kaul-Ghanekar

{"title":"Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines.","authors":"Amrita Ulhe, Prerna Raina, Amol Chaudhary, Ruchika Kaul-Ghanekar","doi":"10.1080/15592294.2025.2451551","DOIUrl":"10.1080/15592294.2025.2451551","url":null,"abstract":"Cervical cancer, the fourth most common cancer globally and the second most prevalent cancer among women in India, is primarily caused by Human Papilloma Virus (HPV). The association of diet with cancer etiology and prevention has been well established and nutrition has been shown to regulate cancer through modulation of epigenetic markers. Dietary fatty acids, especially omega-3, reduce the risk of cancer by preventing or reversing the progression through a variety of cellular targets, including epigenetic regulation. In this work, we have evaluated the potential of ALA (α linolenic acid), an ω-3 fatty acid, to regulate cervical cancer through epigenetic mechanisms. The effect of ALA was evaluated on the regulation of histone deacetylases1, DNA methyltransferases 1, and 3b, and global DNA methylation by ELISA. RT-PCR was utilized to assess the expression of tumor regulatory genes (hTERT, DAPK, RARβ, and CDH1) and their promoter methylation in HeLa (HPV18-positive), SiHa (HPV16-positive) and C33a (HPV-negative) cervical cancer cell lines. ALA increased DNA demethylase, HMTs, and HATs while decreasing global DNA methylation, DNMT, HDMs, and HDACs mRNA expression/activity in all cervical cancer cell lines. ALA downregulated hTERT oncogene while upregulating the mRNA expression of TSGs (Tumor Suppressor Genes) CDH1, RARβ, and DAPK in all the cell lines. ALA reduced methylation in the 5' CpG island of CDH1, RARβ, and DAPK1 promoters and reduced global DNA methylation in cervical cancer cell lines. These results suggest that ALA regulates the growth of cervical cancer cells by targeting epigenetic markers, shedding light on its potential therapeutic role in cervical cancer management.","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2451551"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS. 间质干细胞介导的线粒体转移促进ARDS内皮细胞的代谢重编程和血管再生。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-13 DOI: 10.1080/13510002.2025.2474897

Jinlong Wang, Shanshan Meng, Yixuan Chen, Haofei Wang, Wenhan Hu, Shuai Liu, Lili Huang, Jingyuan Xu, Qing Li, Xiaojing Wu, Wei Huang, Yingzi Huang

{"title":"MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS.","authors":"Jinlong Wang, Shanshan Meng, Yixuan Chen, Haofei Wang, Wenhan Hu, Shuai Liu, Lili Huang, Jingyuan Xu, Qing Li, Xiaojing Wu, Wei Huang, Yingzi Huang","doi":"10.1080/13510002.2025.2474897","DOIUrl":"10.1080/13510002.2025.2474897","url":null,"abstract":"Background: Mesenchymal stem cells (MSCs) are a potential therapy for acute respiratory distress syndrome (ARDS), but their mechanisms in repairing mitochondrial damage in ARDS endothelial cells remain unclear.Methods: We first examined MSCs' mitochondrial transfer ability and mechanisms to mouse pulmonary microvascular endothelial cells (MPMECs) in ARDS. Then, we investigated how MSC-mediated mitochondrial transfer affects the repair of endothelial damage. Finally, we elucidated the mechanisms by which MSC-mediated mitochondrial transfer promotes vascular regeneration.Results: Compared to mitochondrial-damaged MSCs, normal MSCs showed a significantly higher mitochondrial transfer rate to MPMECs, with increases of 41.68% in vitro (P < 0.0001) and 10.50% in vivo (P = 0.0005). Furthermore, MSC-mediated mitochondrial transfer significantly reduced reactive oxygen species (P < 0.05) and promoted proliferation (P < 0.0001) in MPMECs. Finally, MSC-mediated mitochondrial transfer significantly increased the activity of the tricarboxylic acid (TCA) cycle (MD of CS mRNA: 23.76, P = 0.032), and further enhanced fatty acid synthesis (MD of FAS mRNA: 6.67, P = 0.0001), leading to a 6.7-fold increase in vascular endothelial growth factor release from MPMECs and promoted vascular regeneration in ARDS.Conclusion: MSC-mediated mitochondrial transfer to MPMECs activates the TCA cycle and fatty acid synthesis, promoting endothelial proliferation and pro-angiogenic factor release, thereby enhancing vascular regeneration in ARDS.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2474897"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625694","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}

引用次数: 0

Correlation analysis of key genes and immune infiltration in visceral adipose tissue and subcutaneous adipose tissue of patients with type 2 diabetes in women. 女性2型糖尿病患者内脏脂肪组织和皮下脂肪组织关键基因与免疫浸润的相关性分析

IF 3.5 4区生物学

Adipocyte Pub Date : 2025-12-01 Epub Date: 2024-12-24 DOI: 10.1080/21623945.2024.2442419

Qian Shi, Yongxin Li, Chunyan Liu, Mengjie Liang, Hefei Zha, Xin Zhang, Fuchun Zhang

{"title":"Correlation analysis of key genes and immune infiltration in visceral adipose tissue and subcutaneous adipose tissue of patients with type 2 diabetes in women.","authors":"Qian Shi, Yongxin Li, Chunyan Liu, Mengjie Liang, Hefei Zha, Xin Zhang, Fuchun Zhang","doi":"10.1080/21623945.2024.2442419","DOIUrl":"https://doi.org/10.1080/21623945.2024.2442419","url":null,"abstract":"Immune cell infiltration into adipose tissue (AT) is a key factor in type 2 diabetes (T2DM). However, research on the impact of fat distribution on immune cells and immune responses in women is still lacking. This study used enrichment, protein-protein interaction network, immune cell infiltration, and correlation analysis to compare the similarities and differences between the transcriptome data of visceral AT (VAT) and subcutprotein-proteinaneous AT (SAT) obtained from the omprehensive database of gene expression in women with non-T2DM and T2DM. DEGs with the same biological function in two types of ATs often exhibited different expression trends. SharedVAT-specific and SAT-specific hub genes were mainly associated with transcription factors, monocyte-macrophage markers, and chemokines, respectively. Immune cells affected by both AT types included monocytes, granulocytes, T and B lymphocytes, and NK cells. VAT affected more immune cells, mainly myeloid cells. Shared hub genes in VAT correlated positively with M1 macrophages, suggesting pro-inflammatory effects, while those in SAT correlated negatively with M1 macrophages and lymphocytes, suggesting anti-inflammatory effects. This study provides a theoretical basis for further understanding the correlation between AT and T2DM in women.","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"14 1","pages":"2442419"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

tRNA modifications: greasing the wheels of translation and beyond. tRNA修饰：润滑翻译的车轮和超越。

IF 3.6 3区生物学

RNA Biology Pub Date : 2025-12-01 Epub Date: 2024-12-26 DOI: 10.1080/15476286.2024.2442856

Minjie Zhang, Zhipeng Lu

引用次数: 0

Emerging West African Genotype Chikungunya Virus in Mosquito Virome. 蚊子病毒中的新兴西非基孔肯雅病毒基因型。

IF 5.5 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2024-12-23 DOI: 10.1080/21505594.2024.2444686

Pengpeng Xiao, Yujia Hao, Yuge Yuan, Wenzhou Ma, Yiquan Li, He Zhang, Nan Li

引用次数: 0

METTL14 Mediates Glut3 m6A methylation to improve osteogenesis under oxidative stress condition. METTL14介导Glut3 m6A甲基化促进氧化应激条件下的成骨。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-31 DOI: 10.1080/13510002.2024.2435241

Ying Wang, Xueying Yu, Fenyong Sun, Yan Fu, Tingting Hu, Qiqing Shi, Qiuhong Man

{"title":"METTL14 Mediates Glut3 m6A methylation to improve osteogenesis under oxidative stress condition.","authors":"Ying Wang, Xueying Yu, Fenyong Sun, Yan Fu, Tingting Hu, Qiqing Shi, Qiuhong Man","doi":"10.1080/13510002.2024.2435241","DOIUrl":"https://doi.org/10.1080/13510002.2024.2435241","url":null,"abstract":"Objectives: Bone remodeling imbalance contributes to osteoporosis. Though current medications enhance osteoblast involvement in bone formation, the underlying pathways remain unclear. This study was aimed to explore the pathways involved in bone formation by osteoblasts, we investigate the protective role of glycolysis and N6-methyladenosine methylation (m6A) against oxidative stress-induced impairment of osteogenesis in MC3T3-E1 cells.Methods: We utilized a concentration of 200 μM hydrogen peroxide (H2O2) to establish an oxidative damage model of MC3T3-E1 cells. Subsequently, we examined the alterations in the m6A methyltransferases (METTL3, METTL14), glucose transporter proteins (GLUT1, GLUT3) and validated m6A methyltransferase overexpression in vitro and in an osteoporosis model. The osteoblast differentiation and osteogenesis-related molecules and serum bone resorption markers were measured by biochemical analysis, Alizarin Red S staining, Western blot and ELISA.Results: H2O2 treatment inhibited glycolysis and osteoblast differentiation in MC3T3-E1 cells. However, when METTL14 was overexpressed, these changes induced by H2O2 could be mitigated. Our findings indicate that METTL14 promotes GLUT3 expression via YTHDF1, leading to the modulation of various parameters in the H2O2-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model.Discussion: METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2435241"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The highly pathogenic strain of porcine deltacoronavirus disrupts the intestinal barrier and causes diarrhea in newborn piglets. 猪三角冠状病毒的高致病性菌株破坏肠道屏障并引起新生仔猪腹泻。

IF 5.5 1区农林科学

Virulence Pub Date : 2025-12-01 Epub Date: 2025-01-06 DOI: 10.1080/21505594.2024.2446742

Xin Yao, Wei-Hong Lu, Wen-Ting Qiao, Yu-Qian Zhang, Bao-Ying Zhang, Hui-Xin Li, Jin-Long Li

{"title":"The highly pathogenic strain of porcine deltacoronavirus disrupts the intestinal barrier and causes diarrhea in newborn piglets.","authors":"Xin Yao, Wei-Hong Lu, Wen-Ting Qiao, Yu-Qian Zhang, Bao-Ying Zhang, Hui-Xin Li, Jin-Long Li","doi":"10.1080/21505594.2024.2446742","DOIUrl":"https://doi.org/10.1080/21505594.2024.2446742","url":null,"abstract":"Porcine deltacoronavirus (PDCoV) is increasingly prevalent in newborn piglets with diarrhea. With the development of research on the virus and the feasibility of PDCoV cross-species transmission, the biosafety and the development of pig industry have been greatly affected. In this study, a PDCoV strain CH/LNFX/2022 was isolated from diarrheal newborn piglets at a farm in China. A genome-wide based phylogenetic analysis suggests that 97.5% to 99.2% homology existed in the whole genomes of other strains. Five amino acid mutations are seen for the first time in the S protein. By constructing 3D models, it was found that the S1-NTD/CTD and S2-HR-C regions produced structural alterations. Protein functional analysis showed that the structural changes of the three regions changed the epitope of S protein, the O-GalNAc glycosylation site and the 3C-like protease cleavage site. In addition, oral administration of 107 TCID50 CH/LNFX/2022 to newborn piglets successfully reproduced obvious clinical signs of piglets, such as diarrhea and dehydration. Meanwhile, PDCoV antigen was detected by immunofluorescence in the small intestine, and microscopic lesions and intestinal mucosal barrier destruction were detected by histological observation and scanning electron microscopy. Our study confirmed that porcine coronavirus strains increased pathogenicity through evolution, damaged the intestinal barrier of newborn piglets, and caused diarrhea in pigs. This study provided the candidate strains and theoretical basis for establishing the prevention and control system of vaccine and diagnostic methods for piglet diarrhea.","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"16 1","pages":"2446742"},"PeriodicalIF":5.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Remimazolam induced cytotoxicity mediated through multiple stress pathways and acted synergistically with tyrosine kinase inhibitors in hepatocellular carcinoma. 雷马唑仑通过多种应激途径诱导细胞毒性，并与酪氨酸激酶抑制剂协同作用于肝细胞癌。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-07 DOI: 10.1080/13510002.2025.2475696

Hsiu-Lung Fan, Jia-Lin Chen, Shu-Ting Liu, Jia-Tong Lee, Shih-Ming Huang, Zhi-Fu Wu, Hou-Chuan Lai

{"title":"Remimazolam induced cytotoxicity mediated through multiple stress pathways and acted synergistically with tyrosine kinase inhibitors in hepatocellular carcinoma.","authors":"Hsiu-Lung Fan, Jia-Lin Chen, Shu-Ting Liu, Jia-Tong Lee, Shih-Ming Huang, Zhi-Fu Wu, Hou-Chuan Lai","doi":"10.1080/13510002.2025.2475696","DOIUrl":"10.1080/13510002.2025.2475696","url":null,"abstract":"The primary treatment for hepatocellular carcinoma (HCC) involves surgical removal of the primary tumor, but this creates a favorable environment for the proliferation and spread of residual and circulating cancer cells. The development of remimazolam-based balanced anesthesia is crucial for future antitumor applications. It is important to understand the mechanisms of cytotoxicity for HCC in detail.We performed cell viability analysis, western blotting analysis, reverse transcription-polymerase chain reaction analysis, and flow cytometry analysis in two HCC cell lines, HepG2 and Hep3B cells.Our data demonstrated that remimazolam induced cytotoxicity by suppressing cell proliferation, inhibiting G1 phase progression, and affecting mitochondrial reactive oxygen species (ROS) levels, leading to apoptosis, DNA damage, cytosolic ROS elevation, lipid peroxidation, autophagy, mitochondrial depolarization, and endoplasmic reticulum stress. Inhibitors of apoptosis, autophagic cell death, and ferroptosis and a ROS scavenger failed to rescue cell death caused by remimazolam besylate. Our combination index revealed that remimazolam besylate has the potential to act as a sensitizer for targeted tyrosine kinase inhibitor therapy for HCC.Our findings open up new possibilities for combinatory HCC therapy using remimazolam, leveraging its dual functional roles in surgery and drug therapy for liver cancers.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2475696"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575824","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}

引用次数: 0

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