Journal of Bioenergetics and Biomembranes最新文献

{"title":"AURKA regulates HBV-induced hepatic stellate cell inflammation and liver fibrosis by modulating K48-linked ubiquitination and proteasomal degradation of TLR3.","authors":"Hongjie Wu, Tianbao Wang, Fang Yang, Mingqiang Yue, Aihui Li, Changyun Si","doi":"10.1007/s10863-026-10120-2","DOIUrl":"10.1007/s10863-026-10120-2","url":null,"abstract":"<p><p>Chronic hepatitis B (CHB), caused by persistent hepatitis B virus (HBV) infection, continues to pose a major global health threat. Aurora kinase A (AURKA) has been implicated in fibrosis, yet its role in HBV-induced liver fibrosis remains unclear. This study investigated the function and mechanism of AURKA in hepatic stellate cell (HSC) activation and fibrogenesis during CHB. Bioinformatics screening of GSE83148 dataset and validation in human CHB liver specimens, LX-2 HSCs treated with conditioned medium (CM) from HBV-replicating cells, and a persistent HBV recombinant cccDNA (rcccDNA) mouse model established by tail-vein injection of Ad/rcccDNA were performed. Gene and protein expression was analyzed by quantitative PCR and immunoblotting, respectively. Cytokine levels were measured by ELISA. Mitochondrial function was assessed via ROS and JC-1 assays. Protein interactions and ubiquitination were evaluated by co-immunoprecipitation (Co-IP) and protein stability assays. In additional experiments, LX-2 cells were stimulated with purified HBV virions at varying MOIs to assess direct viral effects. AURKA was significantly upregulated in CHB patients and HBV-CM-treated LX-2 HSCs. In LX-2 HSCs, AURKA knockdown attenuated HBV-CM-induced inflammatory cytokine secretion (IL‑1β, IL‑6), mitochondrial dysfunction (mitochondrial ROS, mitochondrial membrane potential), HSC proliferation, and fibrotic marker expression (COL I, α-SMA). Mechanistically, AURKA interacted with TLR3 and was associated with its K48-linked polyubiquitination and degradation. TLR3 silencing abolished the protective effects of AURKA knockdown. In vivo, using a persistent HBV rcccDNA mouse model, AURKA knockdown ameliorated HBV-induced hepatic inflammation and fibrosis by upregulating TLR3. Notably, purified HBV virions alone were sufficient to dose-dependently induce AURKA expression and downstream fibrotic responses in HSCs. This study identifies a novel AURKA/TLR3 axis that regulates HBV-induced HSC activation and liver fibrosis, positioning AURKA as a potential therapeutic target for CHB-associated fibrosis.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470751","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}

{"title":"The role of mitochondrial Na⁺/Ca²⁺ exchanger in brain cell aging.","authors":"Andrey M Khaitin, Alina A Lebedeva, Anastasia E Kunitsyna, Svetlana V Demyanenko","doi":"10.1007/s10863-026-10118-w","DOIUrl":"10.1007/s10863-026-10118-w","url":null,"abstract":"<p><p>Considering the world's population aging and the importance of mitochondrial calcium regulation for all brain pathologies, researchers cannot neglect the role of mitochondrial sodium/calcium exchanger (NCLX) not only in pathologies like Alzheimer's and Parkinson's diseases, but in physiological \"healthy\" aging as well. Despite its critical role in mitochondrial metabolism upon neurodegeneration, the role of NCLX in physiological aging of CNS is almost unknown. NCLX interacts with regulatory partners like TMEM65 and signal pathways of PKA and HIF, connecting to broader metabolic networks of hypoxia, inflammation, oxidative stress, and autophagy. Understanding precise mechanisms of NCLX regulation and its cell-specific roles remains critical for developing targeted interventions to preserve brain function in aging. NCLX is functioning differently in neurons and glial cells, which should be investigated further and considered when studying brain aging. In this review we aim to encompass the current state and connections of this understudied topic and discuss the future prospects and implications.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412001","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}

{"title":"Succinate and lactate produced as conserved biomarkers through chronic and transient substrate-level phosphorylation: from microorganisms to cancer.","authors":"Derek C Lee, Tomas Duraj, Christos Chinopoulos, Thomas N Seyfried","doi":"10.1007/s10863-026-10117-x","DOIUrl":"10.1007/s10863-026-10117-x","url":null,"abstract":"<p><p>ATP is the primary energy currency required by living organisms. Mitochondrial oxidative phosphorylation (OxPhos) produces most of the ATP in quiescent and differentiated cells. OxPhos interruption results in analogous bioenergetic adaptations across divergent evolutionary taxa, yet this adaptation is poorly recognized. Oxygen availability is a major determinant of the source of ATP generation across most eukaryotic cell types. Acute oxygen deprivation, mitochondrial dysfunction, high energy demand, or other metabolic cues can shift relative ATP production from OxPhos to high-throughput fermentation via substrate-level phosphorylations (SLPs). Glucose-derived lactate and glutamine-derived succinate are biomarkers of cytosolic and mitochondrial SLP, respectively. The extracellular accumulation of these metabolites is observed in a broad range of biological systems, including unicellular bacteria and yeast to more complex mammalian cells, including those of the immune system, retina, and muscle. Unsurprisingly, many cancer cells accumulate excess lactate and succinate due to chronic OxPhos insufficiency. This review links ostensibly unique cases of metabolic disruption to the accumulation of lactate and succinate as biomarkers of compensatory fermentative metabolism through cytosolic and mitochondrial SLP. Fundamental principles of cellular energy and environmental adaptation are reviewed that span a broad range of biological complexity.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13337860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sinomenine protects against oxidized low-density lipoprotein-induced human umbilical vein endothelial cell injury through regulating the myocyte enhancer factor 2 A/C-X-C motif chemokine ligand 14 pathway.","authors":"Benbingdi Gong, Bin Wang, Ling Liu, Yifan Yao, Yucheng Wu","doi":"10.1007/s10863-026-10111-3","DOIUrl":"10.1007/s10863-026-10111-3","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a chronic vascular disease characterized by inflammatory response and lipid deposition in the arterial walls caused by endothelial injury. Sinomenine (SIN) could delay AS progression by attenuating endothelial inflammation. However, its role and mechanism in the oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVEC) injury remain unclear. An in vitro model of AS in HUVECs was established using ox-LDL. CCK-8 detected cell viability. ROS, SOD, MDA, TNF-α, IL-β, and IL-6 were evaluated using commercial kits. Western blot was used to detect NLRP3, apoptosis-associated speck-like protein containing ASC, activated caspase-1, GSDMD-N, Arg1, CD206, iNOS, CXCL14, and MEF2A protein levels. CXCL14 mRNA level was measured using RT-qPCR. Binding between MEF2A and CXCL14 promoter was validated using dual-luciferase reporter and ChIP. SIN exposure alleviated ox-LDL-caused oxidative stress, inflammation, pyroptosis, and M1 macrophage polarization in HUVECs. CXCL14 or MEF2A silencing abolished the protective effect of SIN on ox-LDL-caused HUVEC injury. Mechanistically, MEF2A directly interacts with CXCL14 promoter and promotes its transcription. SIN treatment restrained ox-LDL-evoked HUVEC injury and M1 macrophage polarization partly via targeting the MEF2A/CXCL14 axis, providing new insights for future research on the application of SIN in AS treatment.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360990","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}

{"title":"DNMT1 methylates E3 ligase FBXO32 to regulate Myc stability and glycolytic reprogramming in diabetic retinopathy associated endothelial cells.","authors":"Lijuan Zhang, Weiyan Zhou, Yunyan Wu, Bing Wang","doi":"10.1007/s10863-026-10112-2","DOIUrl":"10.1007/s10863-026-10112-2","url":null,"abstract":"<p><p>F-box protein 32 (FBXO32), an E3 ubiquitin ligase, has been implicated in various cellular processes, but its role and regulatory network in DR-associated endothelial dysfunction are unclear. Here, we aimed to investigate the function of FBXO32 in high glucose (HG)-induced vascular endothelial cell injury and the underlying molecular mechanisms mediated by DNMT1 and Myc. Human retinal microvascular endothelial cells (HRMECs) were exposed to HG to mimic DR in vitro. The expression of FBXO32 and DNMT1 was detected by qRT-PCR and Western blot. Gain-of-function and loss-of-function experiments were performed to manipulate FBXO32, DNMT1, and Myc expression. Cell migration was evaluated by wound healing assay. Inflammatory cytokines (IL-1β, IL-6, TNF-α) were measured by ELISA. Glycolytic metabolism was assessed by detecting glucose consumption, lactate production, ATP level, and extracellular acidification rate (ECAR). Co-immunoprecipitation (Co-IP), ubiquitination assay, protein stability assay and GST pull down assay were used to verify the interaction between FBXO32 and Myc. Methylation-specific PCR (MSP) was performed to detect the methylation status of FBXO32 promoter. HG treatment significantly downregulated FBXO32 expression in HRMECs. Overexpression of FBXO32 inhibited HG-induced cell migration, inflammation (decreased IL-6 and TNF-α levels), and glycolytic metabolism (reduced glucose consumption, lactate production, ATP level, and ECAR). Treatment with 2-deoxy-D-glucose (2-DG), a glycolysis inhibitor, abolished the effects of FBXO32 overexpression on cell migration and inflammation, indicating that FBXO32 exerts its function by regulating glycolysis. The interaction between FBXO32 and Myc were confirmed by Co-IP assay and GST pull down assay. Ubiquitination and protein stability assays showed that FBXO32 promotes the ubiquitination and degradation of Myc, thereby reducing Myc protein stability. Overexpression of Myc reversed the inhibitory effects of FBXO32 on HG-induced cell migration, inflammation, and glycolysis. Furthermore, we identified DNMT1 as an upstream regulator of FBXO32. DNMT1 binds to the promoter region of FBXO32 and induces its methylation, leading to the downregulation of FBXO32. Knockdown of DNMT1 upregulated FBXO32 expression, inhibited HG-induced cell migration, inflammation, and glycolysis, while co-knockdown of DNMT1 and FBXO32 reversed these effects. Our findings demonstrate that DNMT1-mediated methylation downregulates FBXO32 expression in HG-induced vascular endothelial cells. FBXO32 inhibits HG-induced endothelial cell migration, inflammation, and glycolytic reprogramming by promoting the ubiquitination and degradation of Myc. This DNMT1-FBXO32-Myc regulatory axis provides a novel therapeutic target for the treatment of DR.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148316891","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}

{"title":"Targeting MEK1/2 inhibits mitochondrial respiration and redox homeostasis in resistant rectal cancer.","authors":"Hu Chenghao, Wu Feng, Chen Chunli, Cai Ting, Li Haixia, Hu Guangyue, Liu Xuefeng, Ma JinLu","doi":"10.1007/s10863-026-10116-y","DOIUrl":"https://doi.org/10.1007/s10863-026-10116-y","url":null,"abstract":"<p><p>Chemo-resistance is a major challenge in rectal cancer treatment. This study investigates the therapeutic potential of MEK inhibitors, cobimetinib and trametinib, in 5-fluorouracil (5-FU)-resistant rectal cancer cells. High-throughput drug screening identified these inhibitors as top candidates based on their selective drug sensitivity scores (sDSS). Both drugs exhibited dose-dependent cytotoxicity against rectal cancer cells while sparing normal epithelial cells and showed synergistic interactions with 5-FU. MEK inhibition disrupted redox homeostasis, increasing reactive oxygen species (ROS) and oxidative damage markers, including protein carbonyl and malondialdehyde (MDA), while also decreasing mitochondrial respiration, as evidenced by reduced oxygen consumption rates (OCR). Apoptotic induction was significantly reduced in mitochondrial respiration-deficient p⁰ cells, supporting the role of mitochondrial respiration in MEK inhibitor activity. Genetic MEK1/2 knockdown mimicked these effects, confirming MEK1/2 as a key regulator of oxidative stress and mitochondrial respiration. In vivo, cobimetinib and trametinib suppressed tumor growth in a chemo-resistant colorectal cancer xenograft model without significant toxicity, inducing oxidative stress and decreasing mitochondrial respiration. These findings highlight MEK inhibitors as promising candidates for overcoming chemo-resistance in rectal cancer by targeting oxidative stress and mitochondrial respiration.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301742","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}

{"title":"Intestinal microecology regulates neutrophil recruitment through TLR4/MAPK/CXCR2 signaling pathway to promote liver ischemia/reperfusion injury.","authors":"Xiaobing Yang, Junbin Zhang, Ningxiang Jiang, Libin Yang, Hongwei Li, Yu Dong, Ying Chen, Rui Chang, Rui Li, Yuanyuan Ma, Yuan Yang, Ping Liu, Peng Song","doi":"10.1007/s10863-026-10115-z","DOIUrl":"10.1007/s10863-026-10115-z","url":null,"abstract":"<p><p>Liver ischemia/reperfusion injury (IRI) is a major complication of hemorrhagic shock, hepatectomy and liver transplantation. Intestinal microecology has momentous functions in various human diseases. The present study aimed to elucidate the role and underlying mechanism of intestinal microecology in liver IRI. A liver IRI mouse model was constructed and validated using hematoxylin and eosin staining, enzyme-linked immunosorbent assay and Naphthol AS-D chloroacetate esterase staining. The function of intestinal microecology in liver IRI was evaluated using flow cytometry and western blot analysis. Moreover, the mechanisms of intestinal microecology in liver IRI were assessed using a series of molecular experiments. The results revealed that liver IRI associated with intestinal microecology dysbiosis exhibited increased hepatic neutrophil infiltration, MAPK pathway activation and inflammatory cytokine production. The 16 S rRNA gene sequencing of fecal samples from Sham, IRI, IRI+antibiotic pre-treatment and fecal transplantation (FT) groups revealed microbial community alterations, with shifts in Bacteroidota and Firmicutes abundance associated with liver injury and neutrophil recruitment. PCA, PCoA and taxonomic profiling further confirmed group-dependent remodeling of the gut microbial community. FT using fecal microbiota from IRI donor mice exacerbated liver neutrophil infiltration, MAPK/CXCR2 activation and inflammatory responses, whereas TAK-242-mediated TLR4 blockade attenuated these effects. Overall, the present study suggests that gut microbiota dysbiosis may enhance liver IRI by promoting neutrophil recruitment, at least in part through the TLR4/MAPK/CXCR2 axis, revealing a novel microbe-immune-liver interaction that may be targeted therapeutically.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148251814","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}

{"title":"Integrating weighted gene co-expression network analysis and machine learning reveal that NDUFA4L2 alleviates KA-induced HT22 cell neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction.","authors":"Huimian Yuan, Wenlong He, Baoshun Du, Jianshe Li","doi":"10.1007/s10863-026-10114-0","DOIUrl":"10.1007/s10863-026-10114-0","url":null,"abstract":"<p><p>Temporal lobe epilepsy (TLE) is one of the most common types of epilepsy, with frequent seizures often leading to cognitive, emotional, and psychiatric issues. A prominent pathological change associated with TLE is hippocampal sclerosis (HS), characterized by neuronal loss, gliosis, and increased neuron fibre density. However, the pathogenesis of Temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) remains unclear. This study aimed to investigate the abnormal expression and regulatory mechanism of hub genes in TLE-HS. The source data were obtained from the epilepsy dataset (GSE256068) of the Gene Expression Omnibus GEO database. Then, differential expression gene (DEG) analysis and weighted gene coexpression network analysis (WGCNA) were employed to screen for module-related DEGs in TLE-HS, followed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Subsequently, these intersected targets were subjected to cross-validation using three machine learning algorithms- LASSO regression, SVM-RFE, and RF, ultimately identifying three hub genes. Finally, CIBERSORT and ssGSEA algorithms were used to analyze the infiltration status of different immune cell populations in TLE-HS patients, followed by assessing the association between hub genes and immune cell populations. The expression of hub genes was determined using RT-qPCR and western blot. Functional experiments were performed using CCK-8, flow cytometry, and special kits. Results indicated that three hub genes, NADH dehydrogenase (ubiquinone) 1 alpha subcomplex subunit 4-like 2 (NDUFA4L2), Protein-tyrosine Phosphatase 4A3 (PTP4A3), and Zinc-alpha-2-glycoprotein (AZGP1), were identified in TLE-HS, which are associated with the infiltration of specific immune cells. Besides, NDUFA4L2 expression was reduced in kainic acid (KA)-induced HT22 cells compared to the other two hub genes. Thus, NDUFA4L2 was selected for this research. Moreover, NDUFA4L2 overexpression alleviated KA‑induced HT22 cell neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction. In conclusion, NDUFA4L2 upregulation could alleviate KA-induced neurotoxicity oxidative stress, which provided a theoretical foundation and a potential therapeutic target for epilepsy.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148198957","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}

{"title":"The FOXO3/ZC3H13/SLC3A2 cascade modulates the osteogenic differentiation and ferroptosis of BMSCs.","authors":"Weifu He, Xiaoyan Shi, Zhengquan Dong, Wenjun Zhang, Lijun Cai, Zhenye Guo, Zhi Lv","doi":"10.1007/s10863-026-10101-5","DOIUrl":"10.1007/s10863-026-10101-5","url":null,"abstract":"<p><p>Impaired osteogenic differentiation in bone marrow-derived mesenchymal stem cells (BMSCs) is involved in the pathogenesis of osteoporosis. ZC3H13, a crucial m6A writer, promotes BMSC osteogenic differentiation by inhibiting ferroptosis. However, its molecular underpinnings remain largely unexplored. Expression analysis was performed by quantitative PCR and immunoblotting. Cell proliferation was assessed by EdU assay. Osteogenic differentiation was assessed using alkaline phosphatase (ALP) expression/activity assays and Alizarin Red staining. Ferroptosis alteration was evaluated by detecting ROS, Fe²⁺, and MDA levels. RNA immunoprecipitation (RIP), methylated RIP (MeRIP), luciferase, and mRNA stability assays were used to validate the regulation of ZC3H13 in SLC3A2. The relationship between FOXO3 and ZC3H13 was confirmed by chromatin immunoprecipitation (ChIP) and luciferase experiments. ZC3H13 was downregulated in the bone marrow of osteoporosis patients. ZC3H13 deficiency inhibited BMSC proliferation and osteogenic differentiation while enhancing ferroptosis. Conversely, ZC3H13 overexpression promoted proliferation, differentiation and suppressed ferroptosis. Mechanistically, ZC3H13 mediated the m6A modification and stability of SLC3A2 in an IGF2BP2-dependent manner. ZC3H13 silencing suppressed BMSC proliferation and osteogenic differentiation while enhancing ferroptosis through SLC3A2 reduction. Furthermore, FOXO3 acted as a transcriptional activator of ZC3H13. Depletion of FOXO3 suppressed BMSC proliferation and osteogenic differentiation while enhancing ferroptosis through downregulation of ZC3H13. Additionally, FOXO3 regulated SLC3A2 expression via ZC3H13. This study delineates a novel FOXO3/ZC3H13/SLC3A2 regulatory cascade that safeguards BMSCs from ferroptosis and is compromised in osteoporosis, providing a new conceptual framework for therapeutic development.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148101348","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}

{"title":"Correction to: Journal of Bioenergetics and Biomembranes Volume 58.","authors":"","doi":"10.1007/s10863-026-10113-1","DOIUrl":"10.1007/s10863-026-10113-1","url":null,"abstract":"","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054651","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}