Antioxidants & redox signaling最新文献

{"title":"Beyond Cys65: Redox Effector Factor-1 CRISPR-Engineered Cys93 and Cys99 Mutants Reveal Cooperative and Secondary Roles of Redox Signaling and Pancreatic Ductal Adenocarcinoma Progression.","authors":"Sanya Haiaty, Jessica A Occhiuto, Eyram Kpenu, Randall S Wireman, Mahmut Mijit, Silpa Gampala, Dana K Mitchell, Xiao Wang, Akanksha Sharma, Rajesh Sardar, Jacqueline Peil, Chi Zhang, Mark R Kelley, Melissa L Fishel","doi":"10.1177/15230864261489484","DOIUrl":"https://doi.org/10.1177/15230864261489484","url":null,"abstract":"<p><strong>Aims: </strong>Apurinic/apyrimidinic endonuclease 1/redox effector factor 1 (APE1/Ref-1) is a multifunctional protein implicated in pancreatic ductal adenocarcinoma (PDAC) through its redox regulation of oncogenic transcription factors (TFs) such as hypoxia-inducible factor 1-alpha, nuclear factor kappa-light-chain-enhancer of activated B cells, and others. While Cys65 is recognized as the primary redox-active residue, the functions of other cysteines remain only partially understood. Here, we describe the first CRISPR-engineered homozygous PDAC cell lines with single (C93A, C99A) and double (C93A + C99A) Ref-1 point mutations. This enabled detailed analysis of the individual and combined roles of Cys93 and Cys99 in Ref-1 redox signaling and their impact on various cancer phenotypes.</p><p><strong>Results: </strong>A single mutation at Cys93 decreased TF activation and reduced tumor cell survival <i>in vitro</i> and <i>in vivo</i>. These effects were similar but less pronounced in cells expressing C99A. The C93A + C99A double mutant further impaired redox signaling and decreased tumor growth and metastasis in orthotopic PDAC mouse models. All of these perturbations specifically disrupted Ref-1's redox activity without impacting its DNA repair function. Due to reduced levels of Ref-1 protein in the C93A + C99A tumor cells, add-back experiments with wild-type Ref-1 and C93A + C99A-Ref-1 examined the impact on cell survival and activation of TFs downstream of Ref-1. Transcriptomic analysis revealed distinct changes in redox and metabolic pathways, although these were less pronounced than those observed with the previously studied C65A mutant.</p><p><strong>Innovation and conclusion: </strong>These findings demonstrate contributory and cooperative, although secondary, roles for Cys93 and Cys99 in Ref-1 redox activity, establish new genetically engineered PDAC models, and underscore the therapeutic potential of targeting Ref-1 redox function in PDAC. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261489484"},"PeriodicalIF":6.8,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148987781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxic Preconditioning Prevents the Neonatal Lung Against Hyperoxia-Induced Ferroptosis Through the Nrf2-CBS Axis.","authors":"Salvador Pérez, Iván Millan, Elena Cubells, Sergio Rius-Pérez, Laura Torrejon, Jaime Ferrer, José M García-Verdugo, Máximo Vento, Isabel Torres-Cuevas","doi":"10.1177/15230864261486899","DOIUrl":"https://doi.org/10.1177/15230864261486899","url":null,"abstract":"<p><strong>Aims: </strong>Hyperoxia-induced oxidative injury contributes to ferroptosis and abnormal lung remodeling in preterm infants receiving oxygen therapy. We previously demonstrated that postnatal hypoxic preconditioning (HP) reduces hyperoxia-induced lung injury in a neonatal mouse model. In the present study, we investigated whether HP protects the neonatal lung against ferroptosis through a nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent mechanism involving transsulfuration and glutathione (GSH) metabolism.</p><p><strong>Results: </strong>In a neonatal mouse model, exposure to HP (FiO₂ = 0.14) prior to hyperoxic challenge (FiO₂ = 1.0) markedly reduced lipid peroxidation, pulmonary ferrous iron accumulation, ferroptosis-associated lipid remodeling, inflammation, and early fibrotic changes in the lung. Mechanistically, HP enhanced antioxidant defenses by increasing Nrf2 activity and promoting transsulfuration-dependent GSH synthesis through upregulation of cystathionine β-synthase (CBS) and xCT, leading to preservation of GSH homeostasis. To determine the functional role of Nrf2, Nrf2 knockout mice were subjected to the same HP/hyperoxia protocol. Nrf2 deficiency abolished the protective effects induced by HP, resulting in increased pulmonary ferrous iron levels, depletion of downstream transsulfuration metabolites and GSH, increased lipid peroxidation, reduced CBS and GPX4 expression, and persistent induction of fibrosis-associated genes.</p><p><strong>Innovation: </strong>This study demonstrates that postnatal HP protects the neonatal lung against hyperoxia-induced ferroptosis through an Nrf2-dependent transsulfuration program. Our findings identify the Nrf2-CBS axis as a key regulator of GSH homeostasis, ferroptosis resistance, and fibrotic remodeling in the developing lung.</p><p><strong>Conclusion: </strong>HP effectively attenuates hyperoxia-induced oxidative stress, ferroptosis, and profibrotic remodeling in neonatal lungs by preserving Nrf2-dependent GSH metabolism and redox homeostasis. These findings support HP as a promising therapeutic strategy to mitigate oxygen-induced pulmonary injury in preterm infants. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261486899"},"PeriodicalIF":6.8,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148987817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Corrigendum to:</i> \"Reactive Oxygen Species-Related Disruptions to Cochlear Hair Cell and Stria Vascularis Consequently Leading to Radiation-Induced Sensorineural Hearing Loss\".","authors":"","doi":"10.1177/15230864261490702","DOIUrl":"https://doi.org/10.1177/15230864261490702","url":null,"abstract":"","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261490702"},"PeriodicalIF":6.8,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148987774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Retraction:</i> \"Lipopolysaccharide-Induced Mitochondrial DNA Depletion\".","authors":"","doi":"10.1177/15230864261485730","DOIUrl":"https://doi.org/10.1177/15230864261485730","url":null,"abstract":"","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261485730"},"PeriodicalIF":6.8,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SGK2 Promotes NEDD4L-Mediated ACSL4 Ubiquitination to Inhibit Ferroptosis and Alleviate Diabetic Kidney Disease.","authors":"Fei Zhang, An-Dong Zhang, Li-Wen Wang, Gui-Yi Liao, Meng Zhang, Ya-Ting Ge, Xin-Ran Liu","doi":"10.1177/15230864261487908","DOIUrl":"10.1177/15230864261487908","url":null,"abstract":"<p><strong>Aims: </strong>Despite major advances with sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists, progressive tubulointerstitial injury remains a major determinant of renal function decline in diabetic kidney disease (DKD), and the molecular regulators of ferroptotic tubular injury remain incompletely defined. Serum/glucocorticoid-regulated kinase 2 (SGK2), predominantly expressed in renal proximal tubular cells, reportedly regulates ferroptosis in prostate cancer; however, its precise role in DKD remains underexplored. Therefore, this study aimed to investigate the role of SGK2 in tubular ferroptosis in DKD.</p><p><strong>Results: </strong>We identified SGK2 as a ferroptosis-related gene through integrated transcriptomic analyses, which was significantly downregulated in renal tubular cells from patients with DKD and diabetic mice. Functional experiments demonstrated that SGK2 overexpression suppressed lipid peroxidation and ferroptosis, thereby alleviating tubular injury, inflammation, and fibrosis. Mechanistically, SGK2 promoted the association of acyl-CoA synthetase long-chain family member 4 (ACSL4) with the E3 ubiquitin ligase neural precursor cell expressed developmentally downregulated 4-like (NEDD4L) and enhanced K48-linked ubiquitination and proteasomal degradation of ACSL4.</p><p><strong>Innovation: </strong>This study identified SGK2 as a novel negative regulator of ferroptosis in patients with DKD. We found that SGK2 suppresses ferroptosis by promoting NEDD4L-mediated ubiquitination and proteasomal degradation of ACSL4, thereby limiting lipid peroxidation and protecting the renal tubules. The SGK2-ACSL4 axis offers new insights into the molecular regulation of tubular ferroptosis.</p><p><strong>Conclusion: </strong>SGK2 suppresses tubular ferroptosis in DKD through NEDD4L-dependent K48-linked ubiquitination and proteasomal degradation of ACSL4. These findings suggest that SGK2 is a potential regulatory target in DKD and provide a basis for further studies on its role in disease progression. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261487908"},"PeriodicalIF":6.8,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bronchopulmonary Dysplasia and the Oxidative Puzzle: Current and New Strategies for Neonatal Health.","authors":"Jiaying Liu, Riyan Huang, Li Fu, Zhenzhuang Zou, Bo Huang","doi":"10.1177/15230864261486341","DOIUrl":"https://doi.org/10.1177/15230864261486341","url":null,"abstract":"<p><p><i>Significance:</i> Bronchopulmonary dysplasia (BPD) remains a major chronic lung disease of prematurity and an important cause of long-term respiratory morbidity in preterm infants. As survival of extremely preterm infants has improved, the clinical burden of BPD has remained substantial. Redox dysregulation, characterized by an imbalance among oxidant exposure, antioxidant capacity, and adaptive signaling responses, represents a central pathogenic mechanism in BPD and contributes to impaired alveolar and vascular development, inflammatory amplification, and defective lung repair.<i>Recent Advances:</i> Current neonatal management strategies, including optimized respiratory support, careful oxygen targeting, nutritional support, caffeine therapy, and selective corticosteroid use, may reduce oxidant burden or modulate redox-sensitive injury pathways. In parallel, antioxidant-related interventions-including vitamins, trace elements, glutathione-related therapies, natural products, and pharmacological agents-have demonstrated biological plausibility.<i>Critical Issues:</i> Current interventions do not consistently correct the underlying redox imbalance of the immature lung. The clinical translation of antioxidant-related therapies remains limited and highly dependent on the level of evidence, intervention timing, and biological context. This review summarizes the role of redox dysregulation in the pathogenesis of BPD and critically examines the clinical and preclinical evidence for redox-related interventions.<i>Future Directions:</i> Emerging priorities include biomarker-guided therapy, omics-informed risk stratification, targeted pulmonary delivery, precision nutritional strategies, and integrated multimodal approaches. Future progress in BPD prevention and treatment will likely depend on integrating redox-informed approaches with established neonatal care, targeted interventions, and rigorous long-term clinical evaluation. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261486341"},"PeriodicalIF":6.8,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148904537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP26 Promotes Autophagosome-Lysosome Fusion to Improve Mitochondrial Function in the Repair of Gut Barrier Damage by Stabilizing STX17.","authors":"Weiming Li, Qinghua Zou, Jiaping Wang, Lili Ding, Hua Yang, Yijun Li, Qingwen Xu, Wenliang Li","doi":"10.1177/15230864261484565","DOIUrl":"https://doi.org/10.1177/15230864261484565","url":null,"abstract":"<p><strong>Aims: </strong>Intestinal mucosal barrier injury is a major consequence of intestinal ischemia-reperfusion (II/R) and contributes to poor clinical outcomes. While mitophagy sustains mitochondrial homeostasis, how impaired autophagic flux disrupts intestinal barrier function remains unclear. We investigated the role of the deubiquitinase ubiquitin-specific protease 26 (USP26) and its downstream target syntaxin 17 (STX17) in regulating mitophagy and intestinal barrier repair.</p><p><strong>Methods: </strong>II/R mouse models and oxygen-glucose deprivation/reperfusion (OGD/R)-treated Caco-2 cells were used to evaluate intestinal barrier integrity. Functional manipulation, autophagy blockade, Co-IP, ubiquitination assays, Seahorse metabolic detection, and <i>in vivo</i> rescue assays were performed to dissect the USP26-STX17 regulatory axis.</p><p><strong>Results: </strong>USP26 was markedly downregulated in II/R intestinal tissues and OGD/R Caco-2 cells, coinciding with impaired autophagy, mitochondrial dysfunction, and intestinal barrier disruption. USP26 overexpression preserved intestinal architecture, reduced permeability and apoptosis, and restored expression of the tight-junction proteins. Functionally, USP26 enhanced autophagic flux and mitophagy, as evidenced by increased LC3-II/LC3-I ratios, reduced p62 accumulation, elevated PINK1/Parkin signaling, improved adenosine triphosphate production, restored mitochondrial membrane potential, and normalized cellular bioenergetics; autophagy inhibition attenuated these protective phenotypes. Mechanistically, USP26 bound STX17 and stabilized it <i>via</i> deubiquitination. STX17 knockdown impaired autophagosome-lysosome fusion and largely abolished USP26-mediated mitochondrial and intestinal barrier protection <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Conclusions: </strong>This study identifies the USP26-STX17 axis as a previously unrecognized regulator of autophagosome-lysosome fusion and mitophagy in II/R injury. By restoring mitochondrial quality control and epithelial barrier integrity, USP26 emerges as a promising therapeutic target for the prevention and treatment of gut barrier dysfunction associated with critical illness. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261484565"},"PeriodicalIF":6.8,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148904751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"uPAR Amplifies Macrophage Inflammation <i>via</i> NF-κB Pathway to Promote Fibrotic Transition Following Acute Kidney Injury.","authors":"Shengchun Zheng, Yan Chen, Jiaona Liu, Na Gong, Yifei Fu, Ziyue Zhang, Lingling Long, Yuanda Wang, Xiangmei Chen, Quan Hong, Xuefeng Sun","doi":"10.1177/15230864261486342","DOIUrl":"https://doi.org/10.1177/15230864261486342","url":null,"abstract":"<p><strong>Aims: </strong>Persistent inflammation is recognized as a major driver of the acute kidney injury (AKI) to chronic kidney disease (CKD) transition, yet upstream macrophage-activation signals remain incompletely understood. Here, we investigated whether the urokinase receptor (uPAR), traditionally linked to matrix remodeling, functions instead as an inflammatory signaling hub that links kidney injury to chronic fibrotic remodeling.</p><p><strong>Results: </strong>In a unilateral renal ischemia-reperfusion injury model, uPAR was induced during the fibrotic phase of postischemic kidney injury. Functional enhancement- and loss-of-function approaches revealed a striking dichotomy: exogenous urokinase (uPA) aggravated renal dysfunction, inflammation, oxidative stress, and fibrosis, whereas uPAR deletion was protective. Mechanistically, uPA/uPAR signaling amplified macrophage inflammatory responses, enhancing M1 polarization, pro-inflammatory cytokine production, reactive oxygen species generation, and NF-κB activation. Molecular docking, mutational modeling, and co-immunoprecipitation analyses revealed a previously underappreciated association between activated uPAR and toll-like receptor 4 (TLR4)-containing complexes. This interaction enhanced myeloid differentiation primary response gene 88-dependent NF-κB signaling and potentiated macrophage inflammatory amplification rather than initiating inflammation independently. NF-κB blockade abolished the pro-inflammatory effects of uPA/uPAR signaling, establishing the functional importance of this pathway.</p><p><strong>Innovation: </strong>We demonstrate that uPA-activated uPAR engages TLR4-associated signaling to intensify macrophage-driven inflammation, oxidative stress, and fibrotic remodeling. These findings redefine uPAR as a molecular switch governing maladaptive kidney repair and identify the uPA/uPAR-TLR4 signaling interface as a promising therapeutic target.</p><p><strong>Conclusion: </strong>Our findings suggest that the uPA/uPAR-TLR4 axis is involved in regulating the progression from AKI to fibrosis. Targeting this signaling node may represent a novel strategy to interrupt maladaptive repair and prevent CKD following AKI. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261486342"},"PeriodicalIF":6.8,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148904608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antihypertensive Agent Alleviates Sodium Hypochlorite-Induced Lung Injury.","authors":"Jiawei Li, Minjie Shi, Gaihua He, Weihua Yu, Zhenpeng Fan, Changyan Wang, Rui Liu, Deqin Kong, Wenjun Li, Jiangzheng Liu, Wenli Li","doi":"10.1177/15230864261484569","DOIUrl":"https://doi.org/10.1177/15230864261484569","url":null,"abstract":"<p><strong>Background: </strong>Bronchial asthma associated with acute or chronic lung injury has emerged as a significant public health concern due to environmental chemical pollution, particularly following the widespread application of sodium hypochlorite (NaClO) disinfectant during the COVID-19 pandemic. Captopril, an antihypertensive agent, has been shown to alleviate symptoms; understanding the mechanism of captopril-mediated protection could facilitate the development of more effective therapeutic strategies. BEAS-2B is a line of immortalized human bronchial epithelial cells, widely used as an <i>in vitro</i> model to investigate pulmonary toxicology. This study investigated the mechanism by which captopril protects the lung and BEAS-2B cells against NaClO-induced lung injury.</p><p><strong>Methods: </strong>Lung injury was induced in mice by NaClO nebulization and in BEAS-2B cells by NaClO treatment. The role of captopril was investigated <i>via</i> physiological monitoring, angiotensin-converting enzyme (ACE) knockdown, and multiomic biochemical analyses focusing on reactive oxygen species (ROS) generation, mitochondrial integrity, and apoptotic/autophagic signaling pathways.</p><p><strong>Results: </strong>Captopril significantly inhibited NaClO-induced apoptosis and suppressed intracellular ROS, reducing oxidative products such as malondialdehyde (MDA) and oxidized glutathione, while simultaneously upregulating the expression of antioxidant enzymes. Furthermore, captopril reduced pro-inflammatory cytokine levels in BEAS-2B cells. It also reduced excessive mitochondrial ROS production and mitigated the NaClO-induced elevation of mitochondrial membrane potential. Notably, the protective effects of captopril were maintained in ACE gene-knockdown BEAS-2B cells, suggesting a potential ACE-independent mechanism. Captopril markedly alleviated NaClO-induced pulmonary injury, specifically improving NaClO-triggered lung dysfunction in mice. Mechanistically, captopril inhibited NaClO-induced apoptosis by upregulating B cell lymphoma 2 (Bcl-2) and downregulating FAS, cleaved caspase 3, and Bcl-2-associated X protein levels. This was linked to captopril suppressing tissue ROS generation, decreasing MDA content, elevating reduced glutathione, and enhancing the expression of antioxidant enzymes. Captopril also alleviated pulmonary and systemic inflammation and regulated autophagy-related proteins, thereby alleviating NaClO-induced dysregulation of autophagy.</p><p><strong>Conclusion: </strong>Together, these findings indicate that captopril holds promise as a potent antioxidant agent to alleviate NaClO-induced lung injury. <i>Antioxid. Redox Signal.</i> 00, 000-000.</p>","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261484569"},"PeriodicalIF":6.8,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WITHDRAWAL-Administrative Duplicate Publication: <i>Corrigendum to:</i> Suppression of Cardiac Autophagy by Hyperinsulinemia in Insulin Receptor-Deficient Hearts Is Mediated by Insulin-Like Growth Factor Receptor Signaling.","authors":"","doi":"10.1177/15230864261483436","DOIUrl":"https://doi.org/10.1177/15230864261483436","url":null,"abstract":"","PeriodicalId":8011,"journal":{"name":"Antioxidants & redox signaling","volume":" ","pages":"15230864261483436"},"PeriodicalIF":6.8,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}