Redox Biology最新文献

{"title":"Corrigendum to \"Nitro-Oleic acid protects from neovascularization, oxidative stress, gliosis and neurodegeneration in oxygen-induced retinopathy\" [Redox Biol. 83 (2025) 103634].","authors":"María Victoria Vaglienti, María Constanza Paz, María Victoria Gutierrez, Paula Virginia Subirada, Jose Luna, Gustavo Bonacci, María Cecilia Sánchez","doi":"10.1016/j.redox.2025.103725","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103725","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":" ","pages":"103725"},"PeriodicalIF":10.7,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3-O-trans-p-coumaroyl esterification enhances the anti-inflammatory effects of tormentic acid by targeting NF-κB signaling","authors":"Mara Heckmann ,&nbsp;Lea Karlsberger ,&nbsp;Bernhard Blank-Landeshammer ,&nbsp;Gerald Klanert ,&nbsp;Nadiia Sadova ,&nbsp;Verena Stadlbauer ,&nbsp;Georg Sandner ,&nbsp;Theresa Gramatte ,&nbsp;Simone Kasis ,&nbsp;Julian Weghuber","doi":"10.1016/j.redox.2025.103731","DOIUrl":"10.1016/j.redox.2025.103731","url":null,"abstract":"<div><div>Tormentic acid (TA), a plant-derived pentacyclic triterpene, exhibits antioxidant and anti-inflammatory potential, yet the pharmacological effects of its 3-<em>O</em>-trans-<em>p</em>-coumaroyl ester (<em>trans</em>-TACE) remain underexplored. This study investigates how hydroxycinnamoyl esterification influences the biological activity of pentacyclic triterpenes by comparing TA and <em>trans</em>-TACE in cellular and <em>in vivo</em> stress models.</div><div>We assessed their ability to mitigate oxidative stress by evaluating the inhibition of ROS and NO molecules. Pro-inflammatory cytokine production in LPS-stimulated THP-1 macrophages was analyzed through cytokine arrays and multiplex immunoassays, while NF-κB activation was examined in both TLR4-dependent and -independent models using HEK-Blue reporter cells. Uptake efficiencies into Caco-2 enterocytes were measured via LC-MS. The <em>in vivo</em> relevance of these findings was assessed using <em>C. elegans</em> as a model for oxidative and inflammatory stress response.</div><div>Results showed that <em>trans</em>-TACE significantly reduced cellular ROS and NO levels compared to TA. Protein analyses of LPS-stimulated THP-1 macrophages indicated that <em>trans</em>-TACE significantly decreased pro-inflammatory cytokines involved in NF-κB signaling (<em>e.g</em>., TNFα, IL-8, CCL2, CXCL5 and CXCL11). <em>Trans</em>-TACE also inhibited NF-κB activation in both TLR4-dependent and -independent models. In <em>C. elegans</em>, both TA and <em>trans</em>-TACE downregulated several stress-induced genes, with <em>trans</em>-TACE exhibiting broader effects by additionally targeting <em>daf-16</em> and <em>gst-4</em> gene expression. Moreover, we revealed key differences in bioactivities between the trans and cis isoform of TACE, underscoring the importance of considering the structural properties of geometric isomers in therapeutic assessments.</div><div>Overall, this study suggests that esterification significantly enhances the biological activity of pentacyclic triterpenes and points towards new possibilities for developing effective natural anti-inflammatory therapies.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103731"},"PeriodicalIF":10.7,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144290970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fructose intake enhances lipoteichoic acid-mediated immune response in monocytes of healthy humans","authors":"Raphaela Staltner,&nbsp;Katja Csarmann,&nbsp;Amelie Geyer,&nbsp;Anika Nier,&nbsp;Anja Baumann,&nbsp;Ina Bergheim","doi":"10.1016/j.redox.2025.103729","DOIUrl":"10.1016/j.redox.2025.103729","url":null,"abstract":"<div><div>Metabolic diseases like type 2 diabetes are afflicted with higher rates of infections and longer, more complicated infection course as well as higher fatality rates. The impact of nutrition and specific nutrients like free fructose herein has not yet been fully understood. Here, we performed dietary intervention studies in healthy individuals and performed <em>ex vivo</em> experiments in isolated blood immune cells to assess the effects of dietary fructose intake on Gram-positive bacterial toxin induced immune responses. Acute and extended intake of fructose but not glucose was related with an induction of <em>Toll like receptor</em> 2 mRNA expression in monocytes and enhanced the LTA-dependent release of proinflammatory cytokines from monocytes. Blocking fructose metabolism and transcription factor SP1 attenuated the fructose-related induction of <em>Toll like receptor</em> 2 mRNA expression and augmentation of proinflammatory cytokine release further suggesting that fructose-dependent metabolic alterations are critical in enhancing immune responsiveness of humans after fructose consumption.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103729"},"PeriodicalIF":10.7,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Guidelines for the measurement of oxygen consumption rate in Caenorhabditis elegans","authors":"Anna Gioran,&nbsp;Niki Chondrogianni","doi":"10.1016/j.redox.2025.103723","DOIUrl":"10.1016/j.redox.2025.103723","url":null,"abstract":"<div><div>Mitochondria are known as the powerhouse of the cell as through oxidative phosphorylation, they produce energy in the form of ATP. Nevertheless, mitochondria are also considered as the main producers of free radicals. Several mitochondrial parameters are needed to be examined to fully characterize mitochondria and the outcomes of their positive (i.e. energy production) or negative (i.e. production of free radicals/oxidative stress) function. Oxygen consumption rate (OCR) measurement is an excellent readout for mitochondrial respiratory capacity and it is the most frequently used assessment to examine mitochondrial function or as part of a broader bioenergetic profiling. Given the link between mitochondrial dysfunction, and increased oxidative stress and damage, and the fact that mitochondrial dysfunction is often reflected in OCR, its measurement is important for the complete characterization of the cellular redox status. Although much of this work is being done in cells or isolated mitochondria, there is an increasing need for the measurement of OCR in whole organismal models such as the nematode <em>Caenorhabditis elegans</em>. As a free-living organism with simple maintenance and conserved mitochondrial biology, <em>C. elegans</em> attracts interest as a model for ageing and age-related diseases, among others, in which bioenergetics but also various mitochondria-related redox aspects need to be evaluated. Therefore, the need for platforms suitable for OCR measurements in this model is evident. In this work, we have employed a newly developed system (Resipher) for the measurement of OCR in <em>C. elegans</em> and we outline basic protocols as well as the pharmacological interventions that can be used to assess the function of the respiratory chain. More specifically, we demonstrate the importance of the number of animals used in measurements that include mitochondrial complex inhibitors, how the presence of bacteria when used as a food source for the nematodes should be carefully considered and/or eliminated and how to avoid artefacts when measuring differently sized nematodes. The present work is not only intended to be used as a protocol for a specific measurement system but it can also be used as a guideline when setting up OCR experiments with any device, as it reveals parameters that may be overlooked and should be carefully considered.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103723"},"PeriodicalIF":10.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 “Autophagy regulates turnover of lipid droplets via ROS-dependent Rab25 activation in hepatic stellate cell” [Redox Biol. 11 (2017) 322–334]","authors":"Zili Zhang ,&nbsp;Shifeng Zhao ,&nbsp;Zhen Yao ,&nbsp;Ling Wang ,&nbsp;Jiangjuan Shao ,&nbsp;Anping Chen ,&nbsp;Feng Zhang ,&nbsp;Shizhong Zheng","doi":"10.1016/j.redox.2025.103717","DOIUrl":"10.1016/j.redox.2025.103717","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"84 ","pages":"Article 103717"},"PeriodicalIF":10.7,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZNFX1 suppresses apoptosis-associated mRNA stability in cardiomyocyte to protect against myocardial infarction","authors":"Yang Shi ,&nbsp;Zeqi Sun ,&nbsp;Yongchao Chen ,&nbsp;Yanli Xie ,&nbsp;Chen Chen ,&nbsp;Han Lou ,&nbsp;Jan Mohammad Omar ,&nbsp;Lei Wang ,&nbsp;Ling Liu ,&nbsp;Heng Liu ,&nbsp;Limin Zhao ,&nbsp;Henghui Xu ,&nbsp;Xiaohan Li ,&nbsp;Run Xu ,&nbsp;Zhouxiu Chen ,&nbsp;Khuzin Dinislam ,&nbsp;Yong Zhang ,&nbsp;Xin Liu","doi":"10.1016/j.redox.2025.103706","DOIUrl":"10.1016/j.redox.2025.103706","url":null,"abstract":"<div><div>Cardiovascular diseases remain a growing global health burden, with myocardial infarction (MI) persisting as the leading cause of cardiovascular mortality worldwide. Zinc finger NFX1-type containing 1 (ZNFX1), an RNA helicase family member, remains relatively understudied in molecular biology and its role in cardiovascular diseases remains unclear. This study aims to explore the involvement of ZNFX1 in MI and uncover its mechanisms. This research found ZNFX1 was decreased in MI myocardium and hypoxia-treated cardiomyocyte. Overexpression of ZNFX1 significantly attenuated myocardial dysfunction, reduced infarct size, inhibited collagen deposition and alleviated cardiac hypertrophy which was ascribed to MI in mice, whereas knockdown of ZNFX1 produced the opposite effects. Mechanistically, RNA-seq identified apoptosis as a possible regulated pathway of ZNFX1, overexpression of ZNFX1 repressed the cardiomyocyte apoptosis that gives rise to MI while knockdown of ZNFX1 deteriorated it. Given the structural similarity between ZNFX1 and UPF1 that confers RNA decay functionality, an in-depth investigation is needed to understand the collective impact of ZNFX1-mediated RNA decay on the process of apoptosis. Here, we report that ZNFX1 plays a protective role in MI by degrading mRNA of apoptosis-related genes, which possess highly structured 3′UTRs. Collectively, this study provides a novel insight into the regulatory mechanisms of programmed cell death, potentially uncovering new targets for therapeutic intervention in diseases where apoptosis is a critical factor.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103706"},"PeriodicalIF":10.7,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of redox homeostasis by ATF4-MTHFD2 axis during white adipose tissue browning","authors":"Rehna Paula Ginting ,&nbsp;Hoang-Anh Pham-Bui ,&nbsp;Choijamts Munkhzul ,&nbsp;Siti Aisyah Fuad ,&nbsp;Ahyeon Son ,&nbsp;Jong-Seok Moon ,&nbsp;Jaeseok Han ,&nbsp;Mihye Lee ,&nbsp;Min-Woo Lee","doi":"10.1016/j.redox.2025.103715","DOIUrl":"10.1016/j.redox.2025.103715","url":null,"abstract":"<div><div>Maintaining redox balance is crucial for mitochondrial homeostasis. During browning of white adipocytes, both the quality and quantity of mitochondria undergo dramatic changes. However, the mechanisms controlling the redox balance in the mitochondria during this process remain unclear. In this study, we demonstrate that thermogenic activation occurs before mitochondrial biogenesis during cold-induced browning of inguinal white adipose tissue (iWAT) and is accompanied by increased mitochondrial stress and integrated stress response (ISR) signaling. Specifically, cold exposure enhances the expression of ATF4, an ISR effector. Adipocyte-specific deletion of ATF4 results in increased energy expenditure, but paradoxically leads to a lower core body temperature, and heightened pro-inflammation in iWAT after cold exposure, which is restored by the antioxidant, MitoQ. Mechanistically, ATF4 regulates the redox balance through MTHFD2, an enzyme involved in mitochondrial redox homeostasis by NADPH generation. Cold exposure upregulates MTHFD2 expression in an ATF4-dependent manner, and its inhibition by DS18561882 <em>in vivo</em> leads to impaired cold-induced mitochondrial respiration similar to the effects of ATF4 loss. These findings suggest that ATF4 is essential for redox balance via MTHFD2, thereby affecting tissue homeostasis during iWAT browning.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103715"},"PeriodicalIF":10.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144271732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uremic toxin receptor NR1H3 contributes to hyperlipidemia- and chronic kidney disease-accelerated vascular inflammation, which is partially suppressed by novel YBX2 anti-ROS pathway","authors":"Yifan Lu ,&nbsp;Yu Sun ,&nbsp;Fatma Saaoud ,&nbsp;Keman Xu ,&nbsp;Ying Shao ,&nbsp;Baosheng Han ,&nbsp;Xiaohua Jiang ,&nbsp;Laisel Martinez ,&nbsp;Roberto I. Vazquez-Padron ,&nbsp;Sadia Mohsin ,&nbsp;Huaqing Zhao ,&nbsp;Hong Wang ,&nbsp;Xiaofeng Yang","doi":"10.1016/j.redox.2025.103724","DOIUrl":"10.1016/j.redox.2025.103724","url":null,"abstract":"<div><div>Hyperlipidemia and chronic kidney disease (CKD) are well-established risk factors for cardiovascular disease and act synergistically to promote vascular inflammation and disease progression. However, the mechanisms underlying this synergetic effect remain largely unknown. Using a mouse model combining hyperlipidemia (via high-fat diet feeding, HFD) with 5/6 nephrectomy-induced CKD, we made the following significant findings: 1) HFD + CKD upregulated 1179 genes in mouse aortas and induced prominent reactive oxygen species (ROS), far more than either HFD or CKD alone. 2) HFD + CKD upregulated 86 CRISPRi-identified mitochondrial ROS regulators, 36 CRISPRi-identified cellular ROS regulators, and 19 GSEA-collected ROS regulators. These changes were associated with the upregulations of 48 cytokines, 7 highest toxicity uremic toxin receptors—including CD1D, FCGRT, AHR, IL6RA AGER, NR1H3 and NPY5R—in aortas. 3) These uremic toxin receptors emerged as novel promoters of inflammation and trained immunity. Deficiencies in CD1D, AHR, AGER, and the trained immunity promoter SET7 each downregulated up to 5.5 % of the genes upregulated by HFD + CKD. Conversely, activation of NR1H3 using an agonist upregulated up to 12.2 % of these genes. 4) The expression of 46 cytokine genes was strongly associated with NR1H3 upregulation. 5) The NR1H3 agonist also induced the expression of 28 ROS regulators, including YBX2, a novel anti-ROS transcription factor and RNA-binding protein, suggesting a potential negative feedback mechanism. YBX2 deficiency increased the cellular ROS level, while YBX2 overexpression suppressed 27 proinflammatory genes induced by HFD + CKD. Our findings provide novel insights into the role of the NR1H3-YBX2 axis in regulating inflammation accelerated by hyperlipidemia and CKD.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103724"},"PeriodicalIF":10.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TSPAN15 sustains ITGB1 stability to block gemcitabine-induced ferroptosis in pancreatic ductal adenocarcinoma through the FAK/AKT/Mtor-gpx4 cascade","authors":"Peng Nan ,&nbsp;Xiao Wang ,&nbsp;Anan Li ,&nbsp;Yumei Ge ,&nbsp;Zongting Gu ,&nbsp;Yingying Wang ,&nbsp;Ran Tao","doi":"10.1016/j.redox.2025.103721","DOIUrl":"10.1016/j.redox.2025.103721","url":null,"abstract":"<div><div>Chemotherapy remains a pivotal strategy in the treatment of pancreatic ductal adenocarcinoma (PDAC). Nonetheless, the emergence of drug resistance has limited the clinical efficacy of chemotherapeutic agents, especially gemcitabine. Here, we identified tetraspanin-15 (TSPAN15), a member of the tetraspanin family, that is frequently overexpressed in human PDAC and is correlated with tumor progression and poor prognosis. Elevated levels of TSPAN15 are involved in mediating gemcitabine resistance of in cancer cells, primarily by inhibiting ferroptosis. Knocking down TSPAN15 increases the sensitivity of PDAC cells to gemcitabine in vitro and in vivo by increasing the susceptibility of cancer cells to ferroptosis. Mechanistically, TSPAN15 directly interacts with integrin-β1 (ITGB1) and maintains its stability by inhibiting ITGB1 ubiquitination. This interaction activates the downstream <em>p</em>-FAK/p-AKT/p-mTOR axis and promotes the expression of glutathione peroxidase 4 (GPX4), a central negative regulator of ferroptosis, ultimately attenuating gemcitabine-induced ferroptosis in PDAC cells. Venetoclax, a newly identified targeted inhibitor of TSPAN15, exhibits synergistic efficacy when combined with gemcitabine for treating PDAC both in vitro and in vivo. This study reveals, for the first time, a major clinically relevant chemoresistance mechanism in PDAC mediated by TSPAN15 in sustaining ITGB1/p-FAK/p-AKT/p-mTOR-GPX4 signaling and tuning ferroptosis, revealing its potential as a viable therapeutic target for chemosensitization.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103721"},"PeriodicalIF":10.7,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Supplementing sialic acid analogs overcomes radiotherapy resistance in triple-negative breast cancer by exacerbating ER stress","authors":"Muwen Yang ,&nbsp;Dongni Shi ,&nbsp;Jianbo Lyu ,&nbsp;Yibing Pan ,&nbsp;Yiyang Lyv ,&nbsp;Xiangfu Chen ,&nbsp;Ying Ouyang ,&nbsp;Yajie Liu ,&nbsp;Yue Li ,&nbsp;Libing Song","doi":"10.1016/j.redox.2025.103712","DOIUrl":"10.1016/j.redox.2025.103712","url":null,"abstract":"<div><div>Radiotherapy is a cornerstone treatment for triple-negative breast cancer (TNBC), and its incorporation has significantly delayed tumor recurrence. However, the emergence of radiotherapy resistance remains a major clinical challenge, substantially compromising treatment efficacy. Sialylation play a pivotal role in tumor therapeutic resistance which refers to the covalent linkage of sialic acids at the terminal ends of glycoproteins, a process catalyzed by a family of sialyltransferases. However, the function and mechanisms of sialylation in radiotherapy resistance remain elusive. In this study, upregulation of Galbeta1-4 GlcNAc alpha 2,3 sialyltransferase (ST3GAL4) was observed in association with sialylation in TNBC patients with radiotherapy resistance and predicted poorer survival. ST3GAL4 catalyzed α2,3-sialylation of HSP90B1, then facilitates its retrograde trafficking from the Golgi to ER mediated by SURF4 cargo receptor. ER-localized HSP90B1 accelerates the clearance of radiotherapy-induced misfolded proteins and upregulates the PERK-EIF2α-ATF4 pathway, which further transcriptionally upregulates antioxidant factors, such as SLC1A5, GCLC, and CTNS, to inhibit radiotherapy-induced ROS accumulation, ultimately leading to radiotherapy resistance, and poor clinical outcomes. Most importantly, sialic acid analogs (SAA) 3Fax-NeuAc inhibited the sialylation of HSP90B1 and its transport to the ER, thereby effectively overcomed radiotherapy resistance in TNBC. This study suggests that ST3GAL4 confers radiotherapy resistance through the induction of adaptive ER stress by sialylated HSP90B1, while the application of SAA provides a novel therapeutic option against radioresistance of TNBC.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"85 ","pages":"Article 103712"},"PeriodicalIF":10.7,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}