Cell Biology and Toxicology最新文献

{"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}

{"title":"Therapeutic implications of endoplasmic reticulum stress gene CCL3 in cervical squamous cell carcinoma.","authors":"Yingping Zhu, Wei Xu, Yuanfang He, Wenjuan Yang, Siyue Song, Chengping Wen","doi":"10.1007/s10565-024-09949-3","DOIUrl":"10.1007/s10565-024-09949-3","url":null,"abstract":"<p><p>This study investigated ERS-related gene expressions in CESC, identifying two molecular subtypes, P1 and P2, and constructing a precise prognostic model based on these subtypes. TCGA's whole-genome expression profiles were used to recognize these subtypes through the ConsensusClusterPlus method, further refining prognostic models with univariate and Lasso Cox regression analyses validated by the GSE39001 dataset. The study analyzed the expression distribution of ERS marker genes within T cell subgroups using scRNA-seq data (GSE168652), highlighting T cell diversity. The critical role of the CCL3 gene in prognostic models was examined explicitly in CD8 + T cells from healthy individuals and CESC patients. Elevated CCL3 levels were observed in patients' CD8 + T cells compared to healthy controls. Functional experiments involving CCL3 knockdown and overexpression in HeLa and SiHa CESC cell lines were conducted to investigate its impact on cell proliferation, migration, and invasion. These findings were subsequently validated in a nude mouse model. The results demonstrated that suppressing CCL3 inhibited cell proliferation, migration, and invasion significantly, while its overexpression promoted these processes. In the mouse model, CCL3 silencing reduced tumor growth and decreased Ki-67 labeling within the tumor tissues, indicating the therapeutic potential of targeting CCL3 in CESC treatment, possibly through CD8 + T cell regulation. This study contributes new prognostic assessment tools and personalized treatment options for CESC patients, paving the way for more targeted therapies in CESC by discovering the CCL3 gene, presenting significant clinical implications.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"47"},"PeriodicalIF":5.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457033","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":"Trps1 regulates mouse zygotic genome activation and preimplantation embryo development via the PDE4D/AKT/CREB signaling pathway.","authors":"Xia Jiang, Weiwei Xu, Jiandong Sun, Jianmin Lin, Zihang Lin, Xiuli Lian, Shumin Liao, Shanshan Luo, Yue Liu, Shie Wang","doi":"10.1007/s10565-025-09999-1","DOIUrl":"10.1007/s10565-025-09999-1","url":null,"abstract":"<p><p>Despite zygotic genome activation (ZGA) is crucial for early embryonic development, its regulatory mechanism is still unclear in mammals. In the present study, we demonstrate that TRPS1, a maternal factor, plays an essential role in mouse early embryogenesis by regulating the transition from 2-cell to 4-cell embryos during preimplantation development. The absence of Trps1 could leads to impaired ZGA through AKT/CREB signaling pathway. Furthermore, our findings suggest that TRPS1 may modulate the transcription of Pde4d to influence AKT and CREB phosphorylation. Interestingly, compared to Trps1 knockdown alone, co-injection of Trps1 siRNA and Pde4d mRNA significantly enhances the development rate of 4-cell embryos. Collectively, these results indicate a negative involvement of Trps1 in mouse preimplantation embryo development by targeting the PDE4D/AKT/CREB pathway to regulate ZGA.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"48"},"PeriodicalIF":5.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467221","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":"Repair mechanisms of bone system tissues based on comprehensive perspective of multi-omics.","authors":"Honghao Yu, Shize Yang, Tianlong Jiang, Tian Li, Hongmei Duan, Minglei Li","doi":"10.1007/s10565-025-09995-5","DOIUrl":"10.1007/s10565-025-09995-5","url":null,"abstract":"<p><p>Bone disorders affect more than half of the adult population worldwide who may have a poor quality of life and physical independence worldwide. Multi-omic techniques are increasingly adopted and applied to determine the molecular mechanisms of bone tissue repair, providing perspective towards personalized medical intervention. Data from genomics, epigenomics, transcriptomics, proteomics, glycomics, and lipidomics were combined to elucidate dynamic processes in bone repair. In this narrative review, the key role of genetic and epigenetic factors in regulating injured cellular responses is highlighted, and changes in RNA and protein expression during the healing phase, as well as glucolipid metabolism adaptation, are described in detail how the repair process is affected. In a word, the integration of multi-omic techniques in this review not only benefits the comprehensive identification of new biomarkers, but also facilitates the development of personalized treatment strategies of bone disorders to revolutionize regenerative medicine.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"45"},"PeriodicalIF":5.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11836151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143448303","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":"Pan-cancer and multi-omics analysis: NDUFA1 is a potential therapeutic target and prognostic marker for esophageal cancer.","authors":"Rui Yin, Gai Zhou, Guanqi Liu, Xiaoting Hou, Haifeng Yang, Jianxin Ge, Jie Ying","doi":"10.1007/s10565-025-09993-7","DOIUrl":"10.1007/s10565-025-09993-7","url":null,"abstract":"<p><strong>Objectives: </strong>The study examined the NDUFA1 expression and its prognostic value in pan-cancer, especially in esophageal cancer (ESCA). Its carcinogenic effect on ESCA was further elucidated.</p><p><strong>Materials and methods: </strong>TCGA database was used to examine NDUFA1 expression and its prognostic value in 33 cancer types. GO and KEGG were performed for function and pathway enrichment of NDUFA1-related genes. The carcinogenic effect on ESCA was verified in both KYSE-30 cell and Xenograft mouse model.</p><p><strong>Results: </strong>Abnormal high expression of NDUFA1 was detected in pan-cancer, and related to immune cell infiltration. TCGA database indicated an elevated value of NDUFA1 in ESCA tumor tissues, which was linked to patients' poor prognosis. NDUFA1-related genes were mainly enriched in oxidative stress and immune response in ESCA. NDUFA1 knockdown significantly suppressed ESCA cell proliferation, migration and invasion. Similarly, tumor growth of ESCA xenograft mice was inhibited by NDUFA1 knockdown. Activated PI3K-Akt signaling was detected in both ESCA cell lines and tumor tissues, which was reversed by NDUFA1 knockdown.</p><p><strong>Conclusion: </strong>Multi-omics analysis showed that NDUFA1 might be adopted as a potential therapeutic goal and prognostic indicator for a variety of cancers, especially for ESCA. NDUFA1 knockdown inhibited ESCA tumor growth, which may have the participation of the PI3K/Akt signaling pathway.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"43"},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11821742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398173","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":"Enhancing cardiac repair post-myocardial infarction: a study on GATM/Gel hydrogel therapeutics.","authors":"Te Li, Lijuan Ding, Qiang Wang, Jianing Ma, Shudong Wang","doi":"10.1007/s10565-025-09987-5","DOIUrl":"10.1007/s10565-025-09987-5","url":null,"abstract":"<p><strong>Background and purpose: </strong>Significant advancements in therapeutic approaches are imperative to address the prevalent impact of myocardial infarction (MI) on morbidity and mortality rates worldwide. This study explores the therapeutic potential of GATM/Gel hydrogel, focusing on its ability to enhance cardiac repair and functionality after MI through modulation of inflammatory and repair pathways.</p><p><strong>Experimental approach: </strong>The effects of GATM/Gel hydrogel on cardiac recovery were studied in a murine MI model. HA-CHO and gelatin solutions were mixed in situ using a dual syringe with a static mixing needle, and the resulting hydrogel was applied directly to the epicardium during MI modeling, followed by repositioning of the heart and closure of the thorax. Comprehensive in vivo assessments-including echocardiography, electrocardiography, and histopathological analysis-were combined with molecular techniques such as RT-qPCR, Western blotting, and immunofluorescence to elucidate the underlying mechanisms. Key cellular and molecular changes were tracked, focusing on macrophage polarization, angiogenesis, and modulation of the TNF/TNFR2 signaling pathway.</p><p><strong>Key results: </strong>Employing the GATM/Gel hydrogel led to a substantial improvement in heart function, shown through enhanced ejection fraction and fractional shortening, and reduced infarction size compared to control groups. Mechanistically, the hydrogel promoted the polarization of anti-inflammatory M2 macrophages and stimulated angiogenesis. Moreover, treatment with GATM/Gel hydrogel altered the TNF/TNFR2 pathway, pivotal in mediating inflammatory responses and facilitating myocardial repair. The discoveries highlight the possibility of GATM/Gel hydrogels as an innovative remedy for MI, providing a twofold role in regulating inflammation and fostering recovery.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"44"},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11821695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398224","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}