International Journal of Biochemistry & Cell Biology最新文献

{"title":"Isoimperatorin attenuates renal ischemia-reperfusion injury by targeting DLAT-associated cuproptosis.","authors":"Jiqiang Zhao, Jiquan Zhao, Junlei Ma, Juan Peng, Li Zhao","doi":"10.1016/j.biocel.2026.107072","DOIUrl":"https://doi.org/10.1016/j.biocel.2026.107072","url":null,"abstract":"<p><p>Cuproptosis, a copper-dependent form of regulated cell death, has recently been implicated in the pathogenesis of renal ischemia-reperfusion injury (IRI). Isoimperatorin (ISO), a natural coumarin, possesses nephroprotective properties, yet its effect on cuproptosis remains unknown. Herein, this study demonstrated that ISO administration effectively attenuated renal tubular injury, improved renal function, and reduced copper accumulation in a mouse IRI model. In vitro, ISO alleviated hypoxia/reoxygenation-induced oxidative stress, mitochondrial damage, and cuproptosis susceptibility. Single-cell transcriptomic (scRNA-Seq) analysis revealed that cuproptosis-related genes (e.g. Fdx1 and Slc31a1) exhibited transcriptional alterations. Through RNA sequencing and molecular interaction assays, this research identified dihydrolipoamide S-acetyltransferase (DLAT) as a binding partner of ISO. DLAT overexpression attenuated the protective effects of ISO, whereas the copper chelator tetrathiomolybdate (TTM) partially recapitulated its action. In vivo, ISO and TTM both suppressed IRI-induced DLAT, FDX1, and CTR1 upregulation. Collectively, our findings suggest that ISO attenuates cuproptosis susceptibility through DLAT, providing a mechanistic rationale for targeting the copper-DLAT axis in ischemic kidney injury.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107072"},"PeriodicalIF":3.5,"publicationDate":"2026-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149372066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern for 'Alpha-synuclein overexpression and aggregation exacerbates impairment of mitochondrial functions by augmenting oxidative stress in human neuroblastoma cells' by Pedram Ghafourifar, [Int. J. Biochem. Cell Biol., vol. 41, Issue 10, October 2009, Pages 2015-2024, 10.1016/j.biocel.2009.05.008].","authors":"","doi":"10.1016/j.biocel.2026.107021","DOIUrl":"10.1016/j.biocel.2026.107021","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107021"},"PeriodicalIF":3.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149065725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern for \"The critical interaction of the metallopeptidase PHEX with heparan sulfate proteoglycans\" [Int. J. Biochem. Cell Biol. 40 (2008) 2781-2792].","authors":"","doi":"10.1016/j.biocel.2026.107022","DOIUrl":"10.1016/j.biocel.2026.107022","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107022"},"PeriodicalIF":3.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Rh1 exerts hepatoprotective effects against liver fibrosis through induction of ferroptosis via SLC7A11 inhibition.","authors":"Fei Zhao, Anwei Wei, Zhenzhen Liu, Yipu Zhao, Bowei Liu","doi":"10.1016/j.biocel.2026.107056","DOIUrl":"https://doi.org/10.1016/j.biocel.2026.107056","url":null,"abstract":"<p><p>Liver fibrosis is a critical pathological stage in the progression from chronic liver disease to cirrhosis, and the exploration of preventive agents derived from traditional Chinese medicine offers considerable potential. However, the precise role and molecular mechanism of ginsenoside Rh1 (Rh1) in liver fibrosis remain largely obscure. This study investigated the anti-fibrotic mechanism of Rh1, focusing on ferroptosis. In vitro, Rh1 dose-dependently suppressed the viability of activated hepatic stellate cells (HSCs) and concurrently induced key ferroptosis features. In vivo, Rh1 administration markedly attenuated carbon tetrachloride-induced liver fibrosis, improved histological architecture, and restored liver function. Mechanistically, transcriptomic analysis and molecular validation identified SLC7A11, a core regulator of ferroptosis, as a binding partner of Rh1. Rescue experiments confirmed that the pro-ferroptotic and anti-fibrotic effects of Rh1 were functionally dependent on SLC7A11 inhibition. In conclusion, our findings demonstrated that ginsenoside Rh1 alleviated liver fibrosis by targeting SLC7A11 to promote the ferroptosis in cultured HSCs, unveiling a novel pharmacological mechanism. This work provided a compelling preclinical rationale for developing Rh1 as a promising preventive agent against liver fibrosis.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107056"},"PeriodicalIF":3.5,"publicationDate":"2026-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149327084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Glycogenes mediate the invasive properties and chemosensitivity of human hepatocarcinoma cells\" [Int. J. Biochem. Cell Biol. 45 (2013) 347-358].","authors":"Rui Guo, Lei Cheng, Yongfu Zhao, Jianing Zhang, Chunqing Liu, Huimin Zhou, Li Jia","doi":"10.1016/j.biocel.2026.107024","DOIUrl":"10.1016/j.biocel.2026.107024","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107024"},"PeriodicalIF":3.5,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149301683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \" Caveolin-1 upregulates CD147 glycosylation and the invasive capability of murine hepatocarcinoma cell lines\" [Int. J. Biochem. Cell Biol. 38 (2006) 1584-1593].","authors":"Li Jia, Shujing Wang, Huimin Zhou, Jun Cao, Yichuan Hu, Jianing Zhang","doi":"10.1016/j.biocel.2026.107019","DOIUrl":"10.1016/j.biocel.2026.107019","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107019"},"PeriodicalIF":3.5,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149301675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern for 'FtsZDr, a tubulin homologue in radioresistant bacterium Deinococcus radiodurans is characterized as a GTPase exhibiting polymerization/depolymerization dynamics in vitro and FtsZ ring formation in vivo' by Hari Sharan Misra, [Intern. J. Biochem. Cell Biol., vol. 50, May 2014, Pages 38-46, 10.1016/j.biocel.2014.01.015].","authors":"","doi":"10.1016/j.biocel.2026.106995","DOIUrl":"https://doi.org/10.1016/j.biocel.2026.106995","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"199 ","pages":"106995"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diosgenin suppresses ALOX5 expression through Histone acetyltransferase KAT2A-mediated H3K27ac modification to attenuate macrophage ferroptosis and foam cell formation in atherosclerosis.","authors":"Qun Huang, Huiping Ou, Yuanbin Li, Liqing Li, Wei Zhuo, Hui Lin","doi":"10.1016/j.biocel.2026.107031","DOIUrl":"https://doi.org/10.1016/j.biocel.2026.107031","url":null,"abstract":"<p><strong>Background: </strong>Diosgenin is a steroidal saponin derived from plants, and it exhibits anti-atherogenic properties. Our research objective is to explore the link between macrophage ferroptosis and foam cell formation, and explore the effect and mechanism of Diosgenin on inhibiting Atherosclerosis (AS) by regulating ferroptosis.</p><p><strong>Methods: </strong>ApoE^-/- mouse models of AS were constructed. Histological analysis of atherosclerotic lesions in aortic root was performed. Plasma levels of TC, TG, HDL-C, and LDL-C were assessed. ELISA detected IL-1β, IL-6, and TNF-α levels in serum. Expressions of ALOX5 and KAT2A were detected by RT-qPCR, Western blot and Immunofluorescence staining. CCK-8 was used to detect cell viability. Levels of MDA, GSH, SOD, 4-HNE, LDH and iron content were measured in macrophages by commercial kits. Chromatin immunoprecipitation (ChIP) and luciferase reporter assay were used to assess the binding of KAT2A and H3K27ac enrichment at the ALOX5 promoter.</p><p><strong>Results: </strong>Diosgenin reduced AS lesions and inhibited macrophage ferroptosis in ApoE^{- /-} mice. The inhibitory effects of Diosgenin on foam cell formation were reversed by Erastin treatment. ALOX5 was discovered as a downstream mediator influenced by Diosgenin. Knocking down ALOX5 reversed ox-LDL-induced foam cell formation. The upregulation of ALOX5 negated Diosgenin's inhibitory impact on ox-LDL-induced macrophage ferroptosis. There was a positive correlation and interaction between KAT2A and ALOX5, a relationship also attenuated by Diosgenin. KAT2A promoted ALOX5 expression, and this effect was accompanied by increased H3K27ac enrichment and KAT2A binding at the ALOX5 promoter, suggesting that KAT2A may enhance ALOX5 expression through H3K27ac modification.</p><p><strong>Conclusion: </strong>Diosgenin attenuated macrophage ferroptosis and foam cell formation in AS at least in part by suppressing ALOX5 expression through KAT2A-mediated H3K27ac modification, which provides new therapeutic targets for AS treatment.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"107031"},"PeriodicalIF":3.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149026631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Luteolin prevents hyperoxaluria-induced renal injury by inhibiting crystal deposition and renal inflammation","authors":"Zhenghui Jin ,&nbsp;Shiqing Zhu ,&nbsp;Chengwei Wang ,&nbsp;Tao Wang ,&nbsp;Jihong Liu ,&nbsp;Yue Wu","doi":"10.1016/j.biocel.2026.106909","DOIUrl":"10.1016/j.biocel.2026.106909","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate the protective effects of Luteolin (LUT) against hyperoxaluria-induced renal injury and calcium oxalate (CaOx) crystal deposition, and to explore the underlying molecular mechanisms.</div></div><div><h3>Method</h3><div>The targets related to LUT and kidney stones were screened in a variety of databases, and the potential targets and pathways were identified by network pharmacology. Subsequently, the interaction between LUT and the core targets was verified by molecular docking and molecular dynamics simulation. Finally, a glyoxylate-induced kidney stone mouse model and high oxalate-induced HK2 cells were used to verify the effect and potential mechanism of LUT on kidney stone formation.</div></div><div><h3>Results</h3><div>Network pharmacology identified 223 intersecting targets between kidney stones and LUT, with KEGG enrichment highlighting the PI3K/Akt signaling pathway. Molecular docking revealed a strong binding affinity between LUT and p85α (-6.947 kcal/mol), and molecular dynamics simulations confirmed complex stability after 25 ns. In vivo, LUT significantly reduced renal calcium oxalate (CaOx) crystal deposition and alleviated tissue injury in the mouse model. In vitro, LUT effectively inhibited oxalate-induced PI3K/Akt activation and inflammatory cytokine production in HK-2 cells. Furthermore, CETSA analysis suggested a potential target engagement between LUT and p85α.</div></div><div><h3>Conclusion</h3><div>This study suggests a protective effect of LUT against kidney stone formation at multiple levels. Our results indicate that LUT attenuates renal calcium crystal deposition, potentially through the inhibition of the PI3K/Akt signaling pathway. These findings provide new insights into the use of natural products for the prevention of nephrolithiasis.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"194 ","pages":"Article 106909"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EFNA3-mediated autophagy suppression drives breast cancer proliferation, EMT and metastasis via PI3K/AKT/mTOR axis","authors":"Luoqiang Lin,&nbsp;Yupeng Yang,&nbsp;Zhenlong Zhang,&nbsp;Xihai Chen","doi":"10.1016/j.biocel.2026.106928","DOIUrl":"10.1016/j.biocel.2026.106928","url":null,"abstract":"<div><h3>Background</h3><div>Breast cancer is a major contributor to cancer mortality in women, and progression, metastasis, and therapy resistance remain key clinical challenges. Ephrin-A3 (EFNA3) has been implicated in various cancers, but its role in breast cancer and underlying mechanisms remain unclear.</div></div><div><h3>Objective</h3><div>To investigate the clinical significance, functional role, and underlying mechanisms of EFNA3 in breast cancer progression.</div></div><div><h3>Methods</h3><div>EFNA3 expression was assessed in breast cancer tissues and cell lines using sequencing, GEPIA, immunohistochemistry, and western blot. Cell proliferation, apoptosis, migration, invasion, and autophagy were evaluated using standard functional assays, LC3 staining, TEM, and western blot. The xenograft model was established using BALB/c nude mice. The effect of EFNA3 knockdown was evaluated by measuring tumor volume, weight, and relevant biomarkers.</div></div><div><h3>Results</h3><div>EFNA3 was upregulated in breast cancer tissues and was associated with poor prognosis. Silencing EFNA3 inhibited cell proliferation and metastasis, and induced apoptosis and autophagy. Mechanistically, our data suggest that EFNA3 activates the PI3K/AKT/mTOR pathway, which is accompanied by reduced autophagy and enhanced tumor progression. Moreover, in a xenograft model, EFNA3 knockdown reduced tumor growth, enhanced autophagy, and inhibited the PI3K/AKT/mTOR pathway.</div></div><div><h3>Conclusions</h3><div>Collectively, our findings suggest that EFNA3 may promote breast cancer progression, at least in part, by activating PI3K/AKT/mTOR signaling and suppressing autophagy. EFNA3 may represent a potential prognostic biomarker and therapeutic target, pending further clinical validation.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"194 ","pages":"Article 106928"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147322515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}