Redox Report最新文献

Correction. 修正。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-12 DOI: 10.1080/13510002.2026.2645268

引用次数: 0

Correction. 修正。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-24 DOI: 10.1080/13510002.2026.2648349

引用次数: 0

Sirtuin 5-mediated desuccinylation of PRDX6 inhibits ferroptosis and alleviates sepsis-associated acute kidney injury. Sirtuin 5介导的PRDX6去琥珀酰化抑制铁下垂并减轻脓毒症相关急性肾损伤。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-10 DOI: 10.1080/13510002.2026.2657075

Wenlong Lin, Caitao Dong, Qinhong Jiang, Yuanquan Lou, Long Wang, Ziqi He

{"title":"Sirtuin 5-mediated desuccinylation of PRDX6 inhibits ferroptosis and alleviates sepsis-associated acute kidney injury.","authors":"Wenlong Lin, Caitao Dong, Qinhong Jiang, Yuanquan Lou, Long Wang, Ziqi He","doi":"10.1080/13510002.2026.2657075","DOIUrl":"10.1080/13510002.2026.2657075","url":null,"abstract":"Objectives: To investigate the role of the SIRT5-PRDX6 axis during the pathogenesis of sepsis-associated acute kidney injury (SA-AKI).Methods: In vivo and in vitro sepsis models were established to evaluate oxidative stress and inflammatory responses. High-throughput proteomics analysis identified ferroptosis as a key mechanism underlying SA-AKI. The levels of HMOX1, NQO-1, GPX4, ACSL4, Fe²⁺, IL-1β, TNF-α, MDA, and GSH were measured. SIRT5 knockdown/overexpression experiments were performed in HK-2 cells, and SIRT5-deficient mice were used to explore its regulatory role. Co-immunoprecipitation (Co-IP) and site-directed mutagenesis verified SIRT5-PRDX6 interaction and desuccinylation sites.Results: Ferroptosis was critical in SA-AKI progression. In LPS-induced HK-2 cells, HMOX1, NQO-1, ACSL4, Fe²⁺, IL-1β, TNF-α, and MDA were significantly increased, whereas GSH and GPX4 were downregulated. Treatment with ferrostatin-1 (Fer-1) attenuated ferroptosis and oxidative damage. SIRT5 decreased in a time-dependent manner following LPS stimulation. SIRT5 knockdown exacerbated LPS-induced ferroptosis, whereas SIRT5 overexpression suppressed it. SIRT5 activation alleviated AKI in mice, whereas SIRT5 deficiency aggravated it. Mechanistically, SIRT5 desuccinylated PRDX6 at lysine 209, thereby inhibiting inflammatory and oxidative stress responses, attenuating ferroptosis, and ultimately ameliorating renal injury.Conclusion: The SIRT5-PRDX6 axis regulates SA-AKI pathogenesis by modulating ferroptosis and represents a novel potential therapeutic target.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2657075"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13072693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps. 胆红素通过抑制nox2介导的中性粒细胞胞外陷阱的形成，降低败血症模型的死亡率。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-28 DOI: 10.1080/13510002.2026.2664962

Sang-Jin Kim, Chang Woo Ko, Wan-Seo Kim, Yeon Jun Kang, Chul-Hwan Lee, Won-Woo Lee, Jong-Wan Park

{"title":"Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps.","authors":"Sang-Jin Kim, Chang Woo Ko, Wan-Seo Kim, Yeon Jun Kang, Chul-Hwan Lee, Won-Woo Lee, Jong-Wan Park","doi":"10.1080/13510002.2026.2664962","DOIUrl":"10.1080/13510002.2026.2664962","url":null,"abstract":"Objectives: Sepsis is a life-threatening condition driven by a dysregulated immune response to infection, yet therapeutic options beyond antibiotics and vasopressors remain limited. Neutrophil extracellular traps (NETs) contribute significantly to sepsis-induced tissue injury, and NETosis inhibition has emerged as a potential therapeutic strategy. We hypothesized that the endogenous metabolite bilirubin mitigates inflammation in sepsis by inhibiting NETosis through targeting NOX2.Methods: Two murine sepsis models were used to assess the effects of bilirubin on survival and systemic NETosis. Plasma NET biomarkers were quantified, and primary human neutrophils were used to validate the NETosis-inhibitory activity of bilirubin in vitro. Mechanistic studies included ROS measurements, NOX2 loop C mutational analysis, and inhibition of endocytosis and autophagy to examine how bilirubin modulates NOX2 stability.Results: Bilirubin improved survival and reduced NET biomarkers in both models. It inhibited NETosis in human neutrophils by suppressing ROS-dependent NETosis and promoting the internalization and degradation of NOX2 via endocytosis and autophagy.Discussion: These findings identify bilirubin as an endogenous inhibitor of NETosis. By targeting NOX2 and suppressing NETosis, bilirubin may represent a promising therapeutic candidate for sepsis management.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2664962"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EGCG-loaded nanoparticles attenuate post-SAH white matter injury by targeting HO-1/S100A10 to suppress oxidative stress-induced reactive astrocytes. 负载egcg的纳米颗粒通过靶向HO-1/S100A10抑制氧化应激诱导的反应性星形胶质细胞，减轻sah后白质损伤。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-28 DOI: 10.1080/13510002.2026.2664955

Dongcen Lang, Yanning Zheng, Jing Zhang, Zheng Li, Mengyu Niu, Jian Wang, Xue Wang, Liyong Huang, Jiangyu Xue, Li Li, Ying Chen

{"title":"EGCG-loaded nanoparticles attenuate post-SAH white matter injury by targeting HO-1/S100A10 to suppress oxidative stress-induced reactive astrocytes.","authors":"Dongcen Lang, Yanning Zheng, Jing Zhang, Zheng Li, Mengyu Niu, Jian Wang, Xue Wang, Liyong Huang, Jiangyu Xue, Li Li, Ying Chen","doi":"10.1080/13510002.2026.2664955","DOIUrl":"10.1080/13510002.2026.2664955","url":null,"abstract":"Objective: Subarachnoid hemorrhage (SAH) is associated with high mortality and poor outcomes, which are closely related to white matter injury (WMI). (-)-Epigallocatechin-3-gallate (EGCG) exerts neuroprotective effects by inhibiting oxidative stress-related ferroptosis in astrocytes and improving neurological function. However, the role and mechanism of EGCG in regulating reactive astrocytes (RAs) to alleviate WMI after SAH remain unclear.Methods: A mouse model of SAH was used to evaluate the effects of EGCG-loaded nanoparticles (EGCG-NPs). Western blot, qPCR, and immunofluorescence were performed for biochemical analysis. Neurological function was assessed using neurological deficit scores and the Morris water maze test.Results: Following SAH, HO-1-mediated iron accumulation and ROS production promoted A1/A2 reactive astrocyte polarization, resulting in myelination damage and aggravated WMI. Knockdown of S100A10 inhibited iron-dependent oxidative stress in RAs and attenuated WMI. EGCG-NPs significantly suppressed HO-1/S100A10-mediated iron overload and oxidative stress in both A1 and A2 RAs, thereby alleviating WMI after SAH.Conclusion: EGCG-NPs attenuate SAH-induced WMI by inhibiting the iron overload-activated HO-1/S100A10 axis in RAs, representing a promising therapeutic strategy.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2664955"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inhibition of oxidative stress and the Neuropilin-2-induced neuroinflammatory pathway by EMO ameliorates epileptic seizures in the preclinical model of epilepsy. EMO抑制氧化应激和neuropilin -2诱导的神经炎症通路改善癫痫临床前模型的癫痫发作。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-18 DOI: 10.1080/13510002.2026.2647496

引用次数: 0

Oxidative stress in neurodegeneration: from a simple insult to a dynamic regulator. 神经退行性疾病中的氧化应激：从简单的伤害到动态调节。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-10 DOI: 10.1080/13510002.2026.2654906

Lan Zhang, Xinyue Zhai, Yalong Yan, Lihong Xiang, Yue Zhang, Xinying Zhou, Lianmei Cai, Zixi Tang, Yiyuan Xia

{"title":"Oxidative stress in neurodegeneration: from a simple insult to a dynamic regulator.","authors":"Lan Zhang, Xinyue Zhai, Yalong Yan, Lihong Xiang, Yue Zhang, Xinying Zhou, Lianmei Cai, Zixi Tang, Yiyuan Xia","doi":"10.1080/13510002.2026.2654906","DOIUrl":"10.1080/13510002.2026.2654906","url":null,"abstract":"Objectives: To evaluate the central role of oxidative stress in neurodegenerative diseases, and to explore its dynamic regulatory features, underlying signaling pathways, and molecular mechanisms, as well as advanced technological strategies for antioxidant intervention.Methods: This review comprehensively evaluated existing literature on oxidative stress in neurodegenerative diseases. It analyzed key regulatory pathways (Nrf2, Keap1, AMPK, mTOR) and molecular processes, including ferroptosis, NETosis, and mitochondrial quality control systems, along with oxidative damage to DNA, lipids, and proteins. The review also assessed advanced technological approaches such as subcellular organelle targeting, nanocarrier delivery systems (e.g. gold nanoparticles, liposomes for glutathione delivery), and single-cell/spatial omics technologies (e.g. single-cell redoxomics, spatial transcriptomics).Results: Oxidative stress exhibits dynamic features, generating protective signals in early stages but transitioning into destructive factors later. A major obstacle for current antioxidant therapies is the blood-brain barrier. Breakthrough strategies identified include precision targeting at the subcellular level, functionalized nanoparticles for efficient antioxidant delivery, and the integration of single-cell redoxomics with spatial transcriptomics to identify specific biomarkers and enable personalized treatments.Discussion: By integrating novel molecular mechanisms and advanced technological resources, this review redefines oxidative stress not as a singular event but as a complex, dynamically regulated system in neurodegenerative diseases. This reconceptualization provides new perspectives for developing targeted and personalized therapeutic interventions.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2654906"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13072707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147654762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plasma proteomics implicates NOX-driven redox imbalance in degenerative cervical myelopathy: findings from the Australian MYelopathy Natural History Registry [AO Spine RECODE-DCM research priority number 5]. 血浆蛋白质组学提示退行性颈椎病中nox驱动的氧化还原失衡：来自澳大利亚脊髓病自然历史登记处的研究结果[AO Spine RECODE-DCM研究优先级5]。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-28 DOI: 10.1080/13510002.2026.2649669

Nashwa Najib, Valerie C Wasinger, Ryan O'Hare Doig, Muhammad Alsherbiny, Stone Sima, Ashish D Diwan

{"title":"Plasma proteomics implicates NOX-driven redox imbalance in degenerative cervical myelopathy: findings from the Australian MYelopathy Natural History Registry [AO Spine RECODE-DCM research priority number 5].","authors":"Nashwa Najib, Valerie C Wasinger, Ryan O'Hare Doig, Muhammad Alsherbiny, Stone Sima, Ashish D Diwan","doi":"10.1080/13510002.2026.2649669","DOIUrl":"10.1080/13510002.2026.2649669","url":null,"abstract":"Objectives: To identify disease-relevant pathways and biomarkers in degenerative cervical myelopathy (DCM) patients from the MYelopathy Natural History Registry.Methods: Shotgun bottom-up proteomics (DCM n = 20; controls n = 20) was performed using LC-MS/MS in DDA mode. Peptides were eluted over 90 min on an in-house manufactured C18 column. Differential proteins were validated using parallel reaction monitoring (PRM) on the same instrument over a 60-min gradient. Bioinformatics was conducted in Skyline and ELISA using Ella™.Results: Discovery proteomics highlighted acute phase and cytokine signalling with STAT1/STAT3 involvement. Targeted assays showed higher IL-6 and IFN-γ in DCM, consistent with a pro-inflammatory state. PRM indicated upregulation of NADPH oxidase complex cytochrome b-245 α-chain (p22 phox or CYBA) and glutathione reductase, alongside downregulation of extracellular glutathione peroxidase, a pattern consistent with NOX-driven reactive oxygen species generation and impaired glutathione redox homeostasis. Together, this provides human plasma evidence of systemic redox imbalance in DCM and nominate a mechanistic framework linking cytokine signalling to oxidative stress via NOX activation and disrupted glutathione cycling.Conclusion: Findings support the feasibility of a plasma 'liquid biopsy' to augment diagnosis and monitoring. The modest cohort size and potential confounding by age and adiposity, absolute quantification, multivariate adjustment, and external validation are warranted to establish specificity and clinical utility.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2649669"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147575182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The oxidative stress paradigm in arbovirus infections: mechanisms and therapeutic insights. 虫媒病毒感染中的氧化应激模式：机制和治疗见解。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-04-15 DOI: 10.1080/13510002.2026.2659994

Chang Ke Yee, Rafidah Lani, Pouya Hassandarvish

{"title":"The oxidative stress paradigm in arbovirus infections: mechanisms and therapeutic insights.","authors":"Chang Ke Yee, Rafidah Lani, Pouya Hassandarvish","doi":"10.1080/13510002.2026.2659994","DOIUrl":"10.1080/13510002.2026.2659994","url":null,"abstract":"Background: Arbovirus infections impose a substantial global health burden, further complicated by their ability to induce oxidative stress through excessive generation of reactive oxygen species (ROS). This oxidative stress triggers a cascade that enhances viral replication and dysregulates immune responses, ultimately exacerbating disease pathology.Objective: In this review, we delineate the molecular pathways through which arbovirus-induced ROS activate NF-κB signalling, impair mitochondrial function, and alter the expression of key antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), culminating in inflammatory tissue damage.Discussions: In vitro studies demonstrate that various alkaloids and polyphenols reduce viral load, while N-acetylcysteine has shown the ability to attenuate inflammation and reduce viral titres across both in vitro and in vivo models. Despite these advances, translation to clinical practice is constrained by limited compound bioavailability, variable pharmacokinetics, optimal timing windows, and a lack of standardized redox assays.Conclusion: We propose that targeted redox-modulating strategies, such as integrating genomic and metabolomic profiling, activating Nrf2 pathways, and incorporating advanced imaging techniques, warrant systematic evaluation using rigorous in vivo models and clinical trials. Defining optimal redox-directed interventions has the potential to catalyse the discovery of novel therapeutics that disrupt pro-viral oxidative pathways and improve outcomes in arboviral disease.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2659994"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147692201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ferroptosis inhibition and mitochondrial rescue: a novel mechanism of emodin in rheumatoid arthritis. 抑制铁下垂和线粒体拯救：大黄素治疗类风湿关节炎的新机制。

IF 7.4 2区生物学

Redox Report Pub Date : 2026-12-31 Epub Date: 2026-03-22 DOI: 10.1080/13510002.2026.2646383

Linlan Zhou, Jun Liu, Jing Ren, Dehao Du, Xiaofeng Rong

{"title":"Ferroptosis inhibition and mitochondrial rescue: a novel mechanism of emodin in rheumatoid arthritis.","authors":"Linlan Zhou, Jun Liu, Jing Ren, Dehao Du, Xiaofeng Rong","doi":"10.1080/13510002.2026.2646383","DOIUrl":"10.1080/13510002.2026.2646383","url":null,"abstract":"Objectives: Rheumatoid arthritis (RA) is characterized by chronic synovitis and progressive joint destruction. Ferroptosis has been implicated in RA pathogenesis through synovial iron accumulation and oxidative stress. Glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) are key regulators of ferroptosis, but their specific roles in RA remain incompletely defined. The objective of this research was to explore the therapeutic effects and the mechanisms behind emodin (EMO) in RA.Methods: The therapeutic efficacy and mechanisms of EMO were evaluated in collagen-induced arthritis mice and lipopolysaccharide-stimulated RAW264.7 macrophages. Joint pathology, inflammation, oxidative stress, ferroptosis, and mitochondrial function were analyzed using histology, micro-computed tomography, western blotting, immunohistochemistry, and microscopy. Key targets were identified and validated using molecular dynamics, molecular docking, proteomics, and network pharmacology.Results: EMO alleviated joint inflammation and bone destruction, reduced pro-inflammatory cytokines and oxidative stress, restored iron and mitochondrial homeostasis, and inhibited ferroptosis. Mechanistically, EMO inhibited ferroptosis through the GPX4/ACSL4 axis, as evidenced by increased GPX4 and decreased ACSL4 expression.Conclusions: EMO ameliorates experimental arthritis mainly by suppressing ferroptosis via the GPX4/ACSL4 axis, highlighting ferroptosis as a previously underappreciated therapeutic target in RA and supporting EMO as a potential adjunctive treatment for RA.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2646383"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13007403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0