Targeting Oxidative Stress in Ischemia/Reperfusion Injury

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 April 2026 | Viewed by 126

Special Issue Editor


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Guest Editor
The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and Pancreas Transplantation, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Interests: ischemia-reperfusion injury; oxidative stress; molecular biochemistry; cell biology; immunology; small molecule pharmacokinetics
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Special Issue Information

Dear Colleagues,

Ischemia/reperfusion (I/R) injury is a critical pathological process that occurs across a broad spectrum of clinical scenarios, including myocardial infarction, stroke, organ transplantation, and major trauma. The sudden restoration of blood flow to ischemic tissues triggers an excessive generation of reactive oxygen species (ROS), initiating a complex cascade of redox-dependent signaling pathways. This oxidative burst plays a central role in causing cellular injury, inflammation, immune dysregulation, and ultimately, organ dysfunction.

This Special Issue aims to highlight recent advances in elucidating the role of oxidative stress in the pathophysiology of I/R injury. We welcome original research and reviews that explore novel redox-regulated molecular and cellular mechanisms, innovative antioxidant-based therapeutic strategies, and translational insights from both preclinical models and clinical investigations.

Topics of particular interest include, but are not limited to, the following:

  • Post-transcriptional regulation of redox signaling, including RNA-binding proteins.
  • Crosstalk between oxidative stress and immune responses in hepatic and systemic I/R injury.
  • Mitochondrial dysfunction and redox imbalance during reperfusion.
  • Development of targeted antioxidants or nanomedicine approaches for I/R injury.
  • Biomarkers and diagnostic tools related to oxidative stress in I/R contexts.

Dr. Kenneth J. Dery
Guest Editor

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Keywords

  • ischemia/reperfusion injury
  • reactive oxygen species
  • redox-regulated molecular and cellular mechanism
  • antioxidant-based therapeutic strategies

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Published Papers (1 paper)

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Research

17 pages, 4691 KB  
Article
Vitamin B12 Protects the Exacerbated Ischemia–Reperfusion Injury-Induced Chronic Kidney Disease in Mice with Genetically Increased Elmo1
by Jiayi Zhou, Yuye Wang, John Hagaman, Qing Ma, J. Charles Jennette, Meitong Chen, Xianwen Yi, Yukako Kayashima, Nobuyo Maeda-Smithies and Feng Li
Antioxidants 2025, 14(11), 1277; https://doi.org/10.3390/antiox14111277 (registering DOI) - 24 Oct 2025
Abstract
Ischemia–reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) and a major driver of progression to chronic kidney disease (CKD). Oxidative stress is recognized as a central mediator of this transition. Engulfment and Cell Motility 1 (ELMO1) regulates cytoskeletal remodeling [...] Read more.
Ischemia–reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) and a major driver of progression to chronic kidney disease (CKD). Oxidative stress is recognized as a central mediator of this transition. Engulfment and Cell Motility 1 (ELMO1) regulates cytoskeletal remodeling and reactive oxygen species generation through Rac1 activation, but its contribution to CKD progression remains poorly defined. To investigate this, we established a unilateral renal IRI model in wild-type (WT) and Elmo1-overexpressing (Elmo1H/H) mice and evaluated kidney function one and four months post-IRI. Compared with WT, Elmo1H/H mice developed more severe kidney dysfunction, including an elevated plasma cystatin C and urinary albumin-to-creatinine ratio, reduced estimated glomerular filtration rate (eGFR), and pronounced fibrosis and glomerular injury observed by light and electron microscopy. Molecular analysis confirmed the dysregulation of redox-related pathways by RT-qPCR, with RNA sequencing showing enrichment of oxidative stress signatures. A subset of mice received chronic vitamin B12 (B12) supplementation following IRI to evaluate its therapeutic potential. Vitamin B12 supplementation improved kidney function, reduced fibrosis, preserved glomerular structure, and normalized the expression of antioxidant genes in both groups. These findings identify Elmo1 as a driver of redox-mediated kidney injury and support vitamin B12 as a promising antioxidant therapy for AKI-to-CKD progression. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress in Ischemia/Reperfusion Injury)
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