Pub Date : 2025-12-20DOI: 10.1016/j.redox.2025.103989
Carl P. Soltau, Debottam Sinha, Lakshita P. Patil, Philip M. Moseley, Cassie L. Rayner, Nigel L. Barnett, Derek J. Richard, Steven E. Bottle, Ian H. Frazer, Alexander P. Martyn
{"title":"Redox-Active Nitroxides Enhance Cisplatin Efficacy against Cervical Cancer","authors":"Carl P. Soltau, Debottam Sinha, Lakshita P. Patil, Philip M. Moseley, Cassie L. Rayner, Nigel L. Barnett, Derek J. Richard, Steven E. Bottle, Ian H. Frazer, Alexander P. Martyn","doi":"10.1016/j.redox.2025.103989","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103989","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"29 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784771","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}
Pub Date : 2025-12-20DOI: 10.1016/j.redox.2025.103980
Abigail Rullo, Brenna Flowers, Keacha Chang, An Zhang, Valentina Z. Petukhova, Luke Harding, Sammy Y. Aboagye, Maurizio Bocchetta, Wei Qiu, David L. Williams, Francesco Angelucci, Pavel Petukhov, Irida Kastrati
{"title":"Unravelling the anti-cancer mechanisms elicited by non-covalent thioredoxin reductase inhibitors for triple negative breast cancer therapy.","authors":"Abigail Rullo, Brenna Flowers, Keacha Chang, An Zhang, Valentina Z. Petukhova, Luke Harding, Sammy Y. Aboagye, Maurizio Bocchetta, Wei Qiu, David L. Williams, Francesco Angelucci, Pavel Petukhov, Irida Kastrati","doi":"10.1016/j.redox.2025.103980","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103980","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"1 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784770","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":"Mitochondrial Dynamics and Their Role in the Pathogenesis of Age-Related Macular Degeneration: A Comprehensive Review","authors":"Kai-Yang Chen, Hoi-Chun Chan, Wan-Wan Lin, Chi-Ming Chan","doi":"10.1016/j.redox.2025.103976","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103976","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"7 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796145","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}
Pub Date : 2025-12-19DOI: 10.1016/j.redox.2025.103981
Fan Yang, Ashia Wheeler-Crawford, Alan McIntyre, Giovanni E. Mann, Joern R. Steinert
{"title":"Physiological oxygen levels reset K+ channel activity in human vascular endothelial cells","authors":"Fan Yang, Ashia Wheeler-Crawford, Alan McIntyre, Giovanni E. Mann, Joern R. Steinert","doi":"10.1016/j.redox.2025.103981","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103981","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"93 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784773","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}
Pub Date : 2025-12-16DOI: 10.1016/j.redox.2025.103982
Jia Wei , Eleonora Duregon , Mauro G. Papotti , Thomas Knösel , Martin Bidlingmaier , Silviu Sbiera , Martin Reincke , Tracy Ann Williams
Aldosterone-producing adenomas (APAs) are a major cause of primary aldosteronism (PA). While oxidative stress and steroidogenesis are intricately linked in adrenal disorders, their interplay and mechanistic basis in APA pathogenesis remain to be fully elucidated. Here, by integrating RNA sequencing of oxidative stress-exposed human adrenocortical cells with spatially-resolved transcriptomic profiling of human adrenal sections, we propose a previously unrecognized role for the activator protein-1 (AP-1) transcription factors FOS and JUN as key mediators linking oxidative stress to steroidogenesis in PA. Their expression and activation are spatially restricted, coinciding with regions of elevated oxidative stress. Phosphorylated FOS and JUN were exclusively detected in the adrenal cortex adjacent to functional adenomas (APAs and cortisol-producing adenomas), with negligible levels in cortex adjacent to non-functional adenomas and in normal adrenal cortex. In vitro, oxidative stress induced the upregulation and activation of FOS and JUN. Conversely, co-overexpression of FOS and JUN suppressed key steroidogenic genes (StAR, CYP11B1, CYP11B2), reduced aldosterone and cortisol secretion, and increased reactive oxygen species accumulation. Together, this work demonstrates that FOS and JUN may function in coordinating the redox-steroidogenesis axis, linking molecular changes in the adjacent cortex to tumor function and microenvironmental remodeling.
{"title":"FOS and JUN regulate oxidative stress and steroidogenesis in human aldosterone-producing adenomas","authors":"Jia Wei , Eleonora Duregon , Mauro G. Papotti , Thomas Knösel , Martin Bidlingmaier , Silviu Sbiera , Martin Reincke , Tracy Ann Williams","doi":"10.1016/j.redox.2025.103982","DOIUrl":"10.1016/j.redox.2025.103982","url":null,"abstract":"<div><div>Aldosterone-producing adenomas (APAs) are a major cause of primary aldosteronism (PA). While oxidative stress and steroidogenesis are intricately linked in adrenal disorders, their interplay and mechanistic basis in APA pathogenesis remain to be fully elucidated. Here, by integrating RNA sequencing of oxidative stress-exposed human adrenocortical cells with spatially-resolved transcriptomic profiling of human adrenal sections, we propose a previously unrecognized role for the activator protein-1 (AP-1) transcription factors FOS and JUN as key mediators linking oxidative stress to steroidogenesis in PA. Their expression and activation are spatially restricted, coinciding with regions of elevated oxidative stress. Phosphorylated FOS and JUN were exclusively detected in the adrenal cortex adjacent to functional adenomas (APAs and cortisol-producing adenomas), with negligible levels in cortex adjacent to non-functional adenomas and in normal adrenal cortex. In vitro, oxidative stress induced the upregulation and activation of FOS and JUN. Conversely, co-overexpression of FOS and JUN suppressed key steroidogenic genes (<em>StAR</em>, <em>CYP11B1</em>, <em>CYP11B2</em>), reduced aldosterone and cortisol secretion, and increased reactive oxygen species accumulation. Together, this work demonstrates that FOS and JUN may function in coordinating the redox-steroidogenesis axis, linking molecular changes in the adjacent cortex to tumor function and microenvironmental remodeling.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103982"},"PeriodicalIF":11.9,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145777263","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}
Pub Date : 2025-12-15DOI: 10.1016/j.redox.2025.103977
Wa Li, Zihui Tang, Jiyang Xue
In head and neck squamous cell carcinoma, a "cold" (immune-desert) tumor microenvironment promotes immunosuppression, which is a critical driver of disease recurrence and therapeutic resistance. To address this challenge, we develop an innovative strategy to remodel the tumor immune microenvironment by disrupting intracellular redox balance to induce ferroptosis and immunogenic cell death, synergistically activating STING pathway to facilitating the transition of tumors from a “cold” to a “hot” immunophenotype. In this study, hyaluronic acid-functionalized hollow manganese dioxide nanoparticles loading β-lapachone (hMnL), engineered for targeted chemo-immunotherapy is constructed. In vitro investigations reveal that hMnL induces robust reactive oxygen species (ROS) generation, triggering ferroptosis and immunogenic cell death. Concurrently, Mn2+ ions released from hMnL in response to the acidic tumor microenvironment activate the STING pathway, fostering dendritic cell (DC) maturation and M1 macrophage polarization. Activation of the ferroptosis and immune-related pathways was indicated by transcriptome sequencing, which identified significantly differentially expressed genes (e.g., Fth1, Hmox1, Calr). In vivo, hMnL exhibits superior tumor-targeting efficacy and sustained intratumoral retention, culminating in potent tumor growth suppression. Furthermore, hMnL activates STING pathway in tumor, leading to enhanced CD8+ T cell infiltration, and a marked reduction in regulatory T cell (Treg) populations. Additionally, hMnL also shows good immunoprotective effects and long-term biosafety. These findings establish hMnL as a promising therapeutic platform that integrates targeted chemotherapy with immune modulation, offering a potent strategy to overcome immunosuppression and improve clinical outcomes in cancer.
{"title":"Synergistic STING Activation and Oxidative Cascades-Induced Ferroptosis Drive Tumor Microenvironment Remodeling by Engineered Manganese Nanoreactors","authors":"Wa Li, Zihui Tang, Jiyang Xue","doi":"10.1016/j.redox.2025.103977","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103977","url":null,"abstract":"In head and neck squamous cell carcinoma, a \"cold\" (immune-desert) tumor microenvironment promotes immunosuppression, which is a critical driver of disease recurrence and therapeutic resistance. To address this challenge, we develop an innovative strategy to remodel the tumor immune microenvironment by disrupting intracellular redox balance to induce ferroptosis and immunogenic cell death, synergistically activating STING pathway to facilitating the transition of tumors from a “cold” to a “hot” immunophenotype. In this study, hyaluronic acid-functionalized hollow manganese dioxide nanoparticles loading β-lapachone (hMnL), engineered for targeted chemo-immunotherapy is constructed. <ce:italic>In vitro</ce:italic> investigations reveal that hMnL induces robust reactive oxygen species (ROS) generation, triggering ferroptosis and immunogenic cell death. Concurrently, Mn<ce:sup loc=\"post\">2+</ce:sup> ions released from hMnL in response to the acidic tumor microenvironment activate the STING pathway, fostering dendritic cell (DC) maturation and M1 macrophage polarization. Activation of the ferroptosis and immune-related pathways was indicated by transcriptome sequencing, which identified significantly differentially expressed genes (e.g., <ce:italic>Fth1</ce:italic>, <ce:italic>Hmox1</ce:italic>, <ce:italic>Calr</ce:italic>). <ce:italic>In vivo</ce:italic>, hMnL exhibits superior tumor-targeting efficacy and sustained intratumoral retention, culminating in potent tumor growth suppression. Furthermore, hMnL activates STING pathway in tumor, leading to enhanced CD8<ce:sup loc=\"post\">+</ce:sup> T cell infiltration, and a marked reduction in regulatory T cell (Treg) populations. Additionally, hMnL also shows good immunoprotective effects and long-term biosafety. These findings establish hMnL as a promising therapeutic platform that integrates targeted chemotherapy with immune modulation, offering a potent strategy to overcome immunosuppression and improve clinical outcomes in cancer.","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"15 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145753426","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}
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