Journal of Bioenergetics and Biomembranes最新文献

{"title":"Total favonoids of Desmodium Styracifolium relieve renal ischemia-reperfusion injury by suppressing ferroptosis through P53/SLC7A11/GPX4 signaling pathway.","authors":"Fangchao Yuan, Qiongyao Peng, Qirui Wang, Qiang Tan, Haiyang Tang, Jie Li, Beike Chen","doi":"10.1007/s10863-025-10076-9","DOIUrl":"10.1007/s10863-025-10076-9","url":null,"abstract":"<p><p>Renal ischemia/reperfusion injury (RIRI), a common complication of renal transplantation, partial nephrectomy, and transient hypoperfusion, is a major etiological factor of acute kidney injury (AKI) with limited treatment options. Total flavonoids from Desmodium styracifolium (TFDS), a traditional Chinese medicinal herb used in urinary disorders, have shown promising renoprotective properties. This study aimed to investigate the efficacy of TFDS against RIRI and elucidate its underlying mechanisms, with a particular focus on oxidative stress and ferroptosis. A RIRI model was established in C57BL/6J mice, and the effects of TFDS were evaluated in both in vivo and in vitro hypoxia/reoxygenation (H/R) models. Evaluation of renal function was performed by measuring serum blood urea nitrogen (BUN) and creatinine levels. Histopathological and ultrastructural alterations were examined using hematoxylin-eosin (H&E) staining and transmission electron microscopy (TEM). Oxidative stress and ferroptosis were evaluated by determining glutathione (GSH) levels, malondialdehyde (MDA) content, reactive oxygen species (ROS) levels, and iron accumulation. Potential therapeutic targets and pathways were predicted by network pharmacology and further validated through Western blot (WB) and immunofluorescence analyses. In vivo, TFDS administration markedly improved renal function in RIRI mice, as evidenced by significant reductions in serum BUN and creatinine levels, and attenuated histopathological damage, including tubular epithelial cell loss and mitochondrial structural disruption. TFDS also decreased tissue iron and malondialdehyde (MDA) levels while restoring GSH content, thereby alleviating oxidative stress and ferroptosis. In vitro, TFDS enhanced HK-2 cell viability after hypoxia/reoxygenation injury, reduced intracellular ROS, iron, and MDA accumulation, and preserved mitochondrial morphology. Network pharmacology and molecular docking identified TP53 as a central target, with vicenin-2, schaftoside, and isovitexin exhibiting strong binding affinity to P53. Mechanistically, TFDS downregulated P53 expression and upregulated SLC7A11 and GPX4 both in vivo and in vitro, effects that were abolished by the P53 agonist Kevetrin, confirming the involvement of the P53/SLC7A11/GPX4 axis in TFDS-mediated ferroptosis suppression. TFDS alleviates kidney injury following RIRI by attenuating oxidative stress and suppressing ferroptosis, effects mediated at least in part through modulation of the P53/SLC7A11/GPX4 signaling axis. These findings identify TFDS as a promising therapeutic candidate for ischemic kidney injury and provide mechanistic insight supporting its potential clinical application.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"423-436"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251217","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":"Fisetinidin chloride ameliorates carbon tetrachloride-induced hepatotoxicity in HepaRG cells.","authors":"Zhen-Bo Wang, Yan-Zhen Zhai, Wei-Qian Deng, Xin-Ling Bai, Yuan Long, Khair Ullah, Abdul Sammad, Jian-Hua Feng","doi":"10.1007/s10863-025-10080-z","DOIUrl":"10.1007/s10863-025-10080-z","url":null,"abstract":"<p><p>Liver diseases poses a significant global health burden. This study investigated the hepatoprotective effects of fisetinidin chloride (FC), a natural flavonoid, against carbon tetrachloride (CCl₄)-induced hepatotoxicity in HepaRG cells, a model mimicking human hepatocyte responses. Co-treatment with FC restored cell viability and reduced cellular steatosis, and minimized lactate dehydrogenase leakage, demonstrating membrane stabilization. FC mitigated oxidative stress by reducing mitochondrial reactive oxygen species (ROS) and lipid peroxidation, while enhancing antioxidant defenses through upregulating mitochondrial superoxide dismutase and glutathione. FC preserved mitochondrial function, as evidenced by restored mitochondrial membrane potential (ΔΨm), and modulated apoptosis by upregulating anti-apoptotic BCL2 mRNA and downregulating pro-apoptotic BAX and caspase-3. Flow cytometry analysis confirmed FC's anti-apoptotic effects, reducing apoptotic cell populations. Additionally, FC attenuated CCl₄-induced elevations in aspartate aminotransferase and alanine aminotransferase, markers of hepatocellular injury. Treatment with FC significantly upregulated choline, citric acid, cis-aconitic acid, L-carnitine, L-tryptophan, and gamma-Linolenic acid in CCl₄-induced cells. Conversely, it significantly downregulated glutamate, xanthine, indole acetic acid, succinic acid, hypotaurine, and other metabolites. Pathway enrichment and network analysis of the metabolome demonstrated that FC's protective effects were mediated through the modulation of mitochondrial energy metabolism. Collectively, these findings highlight FC's multifaceted hepatoprotective effects, including attenuation of cellular steatosis, ROS scavenging, mitochondrial stabilization, and apoptosis inhibition. This study underscores FC's potential as a therapeutic candidate worthy of further mechanistic studies, bridging in vitro efficacy with clinical relevance. Further in vivo studies are warranted to validate its pharmacokinetics and translational potential.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"409-422"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145389771","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":"Effects of sini decoction-mediated cellular mitochondrial autophagy on M1 macrophage polarization and its impact on a mouse model of peripheral artery disease.","authors":"Zhe Liu, Luoqin Guo, Li Jin, Yudong Fang","doi":"10.1007/s10863-025-10072-z","DOIUrl":"10.1007/s10863-025-10072-z","url":null,"abstract":"<p><p>This study aimed to investigate the therapeutic effects of Sini Decoction on a murine model of peripheral arterial disease (PAD) and to explore its potential mechanisms of action related to mitochondrial autophagy and M1 macrophage polarization. A total of 36 specific-pathogen-free Kunming mice were used to establish a PAD model and were randomly assigned into four groups: the experimental group (EG, administered Sini Decoction via gavage), the control group (CG, administered rapamycin via gavage), the model group (MG, administered 0.9% sodium chloride solution via gavage), and the normal group (NG, administered 0.9% sodium chloride solution via gavage). Serum inflammatory cytokines, mitochondrial autophagy-related proteins (LC3bII and p62), M1 macrophage markers (iNOS and COX2), key proteins in the mitochondrial autophagy pathway (PINK1 and Parkin), relative mitochondrial DNA (mtDNA) content, and mitochondrial function indicators [oxygen consumption rate (OCR) and extracellular acidification rate (ECAR)] were measured and analyzed. The serum levels of IL-6, IL-1β, TNF-α, IL-10, and MCP-1 were significantly decreased in both the EG and CG compared to the MG (P < 0.05), with the EG showing considerably greater reductions than the CG (P < 0.05). Compared with the CG, the EG exhibited significantly increased protein and mRNA expression levels of LC3bII, p62, iNOS, and COX2 (P < 0.05), considerably elevated mitochondrial OCR, and considerably reduced ECAR (P < 0.05). Additionally, the relative mtDNA content and the percentage of atherosclerotic lesion area were markedly lower in the EG than in the CG (P < 0.05). Moreover, the expression level of PINK1 and Parkin proteins were significantly increased in both the EG and CG compared to the MG (P < 0.05). Sini Decoction demonstrated superior efficacy in ameliorating PAD compared to the autophagy inducer rapamycin. Its therapeutic effects may be associated with the promotion of mitochondrial autophagy and the induction of M1 macrophage polarization.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"437-451"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029998","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":"Inhibition of myocyte-specific enhancer factor 2A (MEF2A) attenuates cardiac fibrosis and improves heart function by regulating the Snail1/RhoA/α-SMA pathway.","authors":"Qianzhu Jiang, Huiting Li","doi":"10.1007/s10863-025-10075-w","DOIUrl":"10.1007/s10863-025-10075-w","url":null,"abstract":"<p><p>Myocardial fibrosis (MF) is a key pathological process driving heart failure, characterized by excessive extracellular matrix (ECM) deposition and impaired cardiac function. Although myocyte-specific enhancer factor 2 A (MEF2A) is implicated in cardiac fibroblast activation, its role in MF remains unclear. We manipulated MEF2A expression in cardiac fibroblasts (CFs) through knockdown and overexpression, and assessed fibrosis markers, migration, and RhoA signaling. Binding of MEF2A to the Snail1 promoter was predicted using JASPAR and validated by chromatin immunoprecipitation (ChIP) and luciferase reporter assays. Rescue experiments with Snail1 overexpression and RhoA inhibition were performed. An angiotensin II (Ang II)-induced MF mouse model was used to evaluate cardiac function by echocardiography and to assess collagen deposition through picrosirius red (PSR) staining. MEF2A was significantly upregulated in Ang II-induced fibrotic hearts and CFs. MEF2A knockdown reduced α-SMA and Col1a1 expression, inhibited CF migration, and suppressed activation of the Snail1/RhoA/α-SMA pathway. ChIP and luciferase assays confirmed the direct binding of MEF2A to the Snail1 promoter. Inhibition of RhoA signaling reversed MEF2A-induced myofibroblast activation and migration. Rescue experiments showed that Snail1 overexpression restored the fibrotic phenotype suppressed by MEF2A knockdown. In vivo, MEF2A knockdown improved left ventricular function, reduced collagen deposition (PSR staining), and lowered heart weight/tibia length ratios. MEF2A promotes myocardial fibrosis by directly activating Snail1 and engages the RhoA/α-SMA pathway. Targeting MEF2A offers a promising therapeutic strategy to attenuate MF and improve heart function.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"365-377"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955224","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":"Fuzheng Huayu recipe inhibits alveolar macrophage M2 polarization and oxidative phosphorylation via METTL3-mediated NDUFA2 m6A modification.","authors":"Yucen Sun, Xinghua Yuan, Weiling Huang, Qiuhong Li, Shanfang Zhang, Yu Hang, Jingyi Huang, Jiaqi Li, Yechang Qian, Wei Zhang, Li Li","doi":"10.1007/s10863-025-10074-x","DOIUrl":"10.1007/s10863-025-10074-x","url":null,"abstract":"<p><p>Clinical evidence points to the Traditional Chinese Medicine Fuzheng Huayu recipe (FZHYR) as an anti-fibrosis drug. Our previous studies have shown that FZHYR regulates macrophage polarization and the expression of NADH dehydrogenase (ubiquinone) 1 alpha subcomplex subunit 2 (NDUFA2) to inhibit pulmonary fibrosis. This study aims to explore the mechanism of FZHYR regulates macrophage polarization and NDUFA2 expression in the treatment of pulmonary fibrosis. NR8383 alveolar macrophages polarizing to M1 or M2 polarization by stimulation with LPS/IFN-γ or IL-14/IL-13 and received FZHYR treatment. Macrophage polarization was verified by detecting the levels of transmembrane protein that specific expression using flow cytometry and levels of inflammatory factors. Oxidative phosphorylation change was reflected by mitochondrial ROS and oxygen consumption rate. The effect of FZHYR on m6A of Ndufa2 mRNA and the involvement of m6A modification enzymes (METTL3 and IGF2BP1) was investigated. FZHYR promoted macrophage M1 polarization and inhibited macrophage M2 polarization. FZHYR inhibited oxidative phosphorylation and NDUFA2 expression in M2 macrophages. Ndufa2 silencing inhibited macrophage M2 polarization and oxidative phosphorylation. M2 macrophage polarization and oxidative phosphorylation induced by Ndufa2 overexpression were reversed by FZHYR. Mechanistically, METTL3 induced Ndufa2 m6A methylation in an IGF2BP1-dependent manner in FZHYR-treated M2 macrophage. Moreover, the inhibition of METTL3 suppressed macrophage M2 polarization and oxidative phosphorylation. FZHYR inhibits M2 macrophage polarization through the inhibition of METTL3-mediated m6A modification and downregulation of NDUFA2 and oxidative phosphorylation.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"453-467"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091844","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":"Astragaloside IV ameliorates cardiomyocyte injury and heart failure through hif/rho/rock pathway regulation: In vitro and in vivo insights.","authors":"Gang Li, Min Wang, Qiufen Dong, Dan Li, Juan Liu, Qi Long, Yanbing Ding","doi":"10.1007/s10863-025-10073-y","DOIUrl":"10.1007/s10863-025-10073-y","url":null,"abstract":"<p><p>Heart failure represents the culmination of various cardiovascular diseases, distinguished by a spectrum of complex symptoms. Astragaloside IV (AST-IV) has shown significant cardiac protection in heart failure rats, though the mechanisms are not fully understood. This study aimed to investigate the effects of AST-IV using hypoxia-reoxygenation injury in cardiomyocytes and heart failure in rats to explore the effects of AST-IV. Experimental groups were treated with AST-IV, HIF-2α siRNA, or Y-27,632 (a ROCK inhibitor). Cell proliferation was assessed using CCK-8 and EdU assays, while mitochondrial membrane potential and apoptosis were evaluated using JC-1 fluorescent probes and TUNEL staining, respectively. Additionally, flow cytometry measured reactive oxygen species and apoptosis rates, with protein expressions of HIF-2α, RhoB, and ROCK determined via western blotting. Cardiac troponin I and caspase-3 levels were quantified using ELISA, and myocardial injury was examined through H&E and Masson staining. Results demonstrated that AST-IV notably increased HIF-2α and Rho/ROCK pathway protein expressions, enhancing cell proliferation, reducing apoptosis and ROS levels, but effects were partially reversible by Y-27,632 in vitro. Our findings suggest that AST-IV mitigates hypoxia-induced cardiomyocyte damage by modulating the HIF/Rho/ROCK pathway, indicating its potential as a therapeutic agent for heart failure.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"351-364"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286139","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":"Interaction of bile acids with functionally active liver mitochondria: uncoupling activity, detergent effect, and antioxidant action.","authors":"Evgeniya K Pavlova, Victor N Samartsev, Svetlana I Pavlova, Mikhail V Dubinin","doi":"10.1007/s10863-025-10077-8","DOIUrl":"10.1007/s10863-025-10077-8","url":null,"abstract":"<p><p>This study investigates the interactions of primary and secondary bile acids (cholic acid (CA), chenodeoxycholic acid (CDCA), ursodeoxycholic acid (UDCA), and lithocholic acid (LCA)) with isolated rat liver mitochondria, focusing on their uncoupling activity, detergent effects, and antioxidant properties. Using a recently developed methodological approach based on quantifying the effective distribution coefficient ([Formula: see text]), we precisely assessed the partitioning of bile acids between the mitochondrial and aqueous phases. Our results demonstrate that the uncoupling potency rank order was LCA > CDCA > CA, which strongly correlated with their lipophilicity. In contrast, UDCA, which possesses hydroxyl groups on the hydrophobic β-surface, exhibited significantly lower uncoupling activity. At concentrations inducing mild uncoupling (stimulating state 4 respiration by 70-75%), all bile acids significantly reduced the ADP/O ratio and respiratory control ratio without inhibiting the electron transport chain, confirming their protonophoric mechanism. Furthermore, we quantitatively showed that bile acids, in contrast to palmitic acid, exert a mild detergent effect, as evidenced by a increase in NADH-stimulated respiration, with UDCA and CA having the most pronounced effect. Crucially, at these uncoupling concentrations, all bile acids consistently suppressed mitochondrial H₂O₂ generation by 30-40%, revealing their antioxidant potential. These findings provide quantitative insights into the structure-dependent dual roles of bile acids in modulating mitochondrial function.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"379-390"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199560","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":"Rab3A attenuated H₂O₂-induced mitochondrial dysfunction and damage in HEI-OC1 cells by stabilizing ITGA3 expression.","authors":"Yanlu Lyu, Daishi Chen, Huihui Liu, Zhaoyang Ke","doi":"10.1007/s10863-025-10079-6","DOIUrl":"10.1007/s10863-025-10079-6","url":null,"abstract":"<p><p>According to reports, Rab3A plays a kay role in various diseases. The regulatory role of Rab3A in hair cell damage and age-related hearing loss has not been explored. HEI-OC-1 cells were treated with hydrogen peroxide (H₂O₂) to construct a damage model. The cell viability and apoptosis were detected by CCK-8 assay and flow cytometry. Immunofluorescence and flow cytometry were used to measure mitochondrial membrane potential. The contents of oxidative stress-related indicators and mitochondrial function-related indicators were detected by kits. Dual luciferase assay was used to determine the regulatory relationship between Rab3A and ITGA3. The results showed that H₂O₂ treatment reduced the level of Rab3A in HEI-OC-1 cells in a time-dependent manner. Rab3A increased the cell viability of H₂O₂-induced inner ear cells and inhibited cell apoptosis. Additionally, Rab3A inhibited H₂O₂-induced oxidative stress and alleviated mitochondrial dysfunction in HEI-OC-1 cells. Rab3A also directly targeted and positively regulated ITGA3 expression. Further studies found that silencing of ITGA3 reversed the inhibitory effects of Rab3A on inner ear cell damage and mitochondrial dysfunction. In conclusion, Rab3A regulates H₂O₂-induced inner ear hair cell damage and mitochondrial dysfunction by stabilizing the expression of ITGA3.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"337-349"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286159","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":"Early cardioprotective effects of SGLT2i on hypertensive cardiac remodeling via STIM1/Orai1-dependent calcium signaling: beyond blood pressure control.","authors":"Jian Wu, Zhuoran Jia, Xiaohe Wu, Yangcheng Xue, Peiyang Zheng, Huimin Wang, Ren Zhao","doi":"10.1007/s10863-025-10067-w","DOIUrl":"10.1007/s10863-025-10067-w","url":null,"abstract":"<p><p>The cardioprotective effects of sodium-glucose cotransporter-2 inhibitors (SGLT2i) have attracted significant attention. The calcium ion signaling pathway influences various aspects of cellular function, store-operated calcium channels (SOCCs) serve as key calcium ion channels that induce cell apoptosis and exacerbate cardiac remodeling. This study aims to investigate the effects of SGLT2i on SOCCs and its potential cardioprotective mechanisms. Sprague-Dawley (SD) rats were sequentially treated with angiotensin II (Ang II) and dapagliflozin (Dapa), randomly divided into four groups: Sham, Dapa, Ang II, and Ang II + Dapa. Blood pressure, cardiac structure and function were measured. Cardiac fibrosis evaluated using Masson's trichrome staining. The apoptosis rate of H9C2 cells was determined by flow cytometry. Protein expression levels and functional activity of SOCCs were analyzed using Western blotting, calcium imaging, and fluorescence co-localization staining. In Ang II-induced hypertension rats, no significant blood pressure lowering effect of Dapa was observed within 28 days. Notably, the absence of blood pressure reduction did not affect the timely improvement of Ang II-induced cardiac remodeling by Dapa. Ang II enhanced store-operated calcium entry (SOCE), subsequently promoting cardiomyocyte apoptosis. Dapa administration effectively suppressed this pathological process by inhibiting the overexpression and overactivation of SOCC. SGLT2i improved early cardiac remodeling induced by Ang II without relying on antihypertensive effects, mainly by inhibiting excessive activation of SOCE, which effectively attenuated Ang II-triggered cardiomyocyte apoptosis. This provides a novel therapeutic paradigm targeting impaired myocardial calcium handling in hypertensive heart disease management.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"245-259"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144731120","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":"TKT regulates the pentose phosphate pathway via RBKS to promote epithelial-mesenchymal transition during AML progression.","authors":"Feifan Li, Jiaqi Liu, Yinghua Geng, Lin Liu, Jun Li, Lianfang Pu, Zhongli Hu, Yanli Yang","doi":"10.1007/s10863-025-10064-z","DOIUrl":"10.1007/s10863-025-10064-z","url":null,"abstract":"<p><p>Acute myeloid leukemia is a life-threaten disease. Researches have indicated that increased expression of TKT was closely related to the progression of malignant tumors. However, the mechanism of TKT in the pathogenesis of AML need to be further elucidated. Here, we showed that the expression levels of TKT was increased in AML patients and AML cells. TKT overexpression in AML cells significantly promoted the proliferation, migration and invasion of cells while TKT knockdown had opposite effects. Mechanistically. We proved that TKT was located on up-stream of RBKS and TKT promoted the growth of AML cells through RBKS. In addition, our data indicated that TKT regulates the pentose phosphate pathway via RBKS. Notably, we demonstrated that the pentose phosphate pathway is crucial for EMT program in AML cells. Taken together, this study identified the molecular mechanism by which TKT promotes AML progression, namely, TKT promotes EMT by regulating the pentose phosphate pathway through RBKS. Our results suggest that TKT maybe a novel therapeutic target for AML treatment.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":"289-302"},"PeriodicalIF":3.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325827","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}