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Journals
Antioxidants
Special Issues
Targeting Oxidative Stress in Ischemia/Reperfusion Injury
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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: 10 November 2026 | Viewed by 4657

Special Issue Editor

Dr. Kenneth J. Dery

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (3 papers)

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Research

24 pages, 1716 KB  
Article
Tacrolimus (FK506) Attenuates Hepatic Ischemia–Reperfusion Injury via Oxidative Glutathione Metabolism and Suppression of Lipoxygenase-Mediated Cell Death
by Moritz Drefs, Malte J. Schirren, Dominik T. Koch, Severin J. Jacobi, Michael Neuberger, Lesca M. Holdt, Bernhard W. Renz, Jens Werner, Markus O. Guba and Dionysios Koliogiannis
Antioxidants 2026, 15(5), 557; https://doi.org/10.3390/antiox15050557 - 28 Apr 2026
Viewed by 426
Abstract
Background: Hepatic ischemia–reperfusion injury (IRI) remains a major challenge in liver transplantation (LTx) and hepatectomy. Previous studies identified a 12/15-lipoxygenase (12/15-LOX)-driven lipid peroxidation cascade promoting cell death, whereas glutathione peroxidase 4 (GPx4)-dependent metabolism acts antagonistically. This study investigated whether tacrolimus protects against hepatic [...] Read more.
Background: Hepatic ischemia–reperfusion injury (IRI) remains a major challenge in liver transplantation (LTx) and hepatectomy. Previous studies identified a 12/15-lipoxygenase (12/15-LOX)-driven lipid peroxidation cascade promoting cell death, whereas glutathione peroxidase 4 (GPx4)-dependent metabolism acts antagonistically. This study investigated whether tacrolimus protects against hepatic IRI through this redox axis. Methods: Male C57BL/6 mice underwent 65% partial hepatic warm ischemia and reperfusion with or without tacrolimus preconditioning. Liver tissue and serum were analyzed by spectral photometry, Western blotting, TUNEL assay, and serum enzyme measurement. Results were statistically analyzed and compared with previously published results of 12/15-LOX inhibition by baicalein pretreatment and its carrier DMSO. Also, the combination of both tacrolimus and baicalein was investigated. Results: Tacrolimus increased the oxidative glutathione activity quotient (GSSG/GSH) by 75.1% (p = 0.0302), attenuated MAPK signaling, reduced SAPK/JNK by 84.6% (p = 0.0059), with ERK1/2 showing a downward trend, decreased Caspase-3 activation by 66.9% (p < 0.001) and PARP cleavage by 59.9% (p = 0.0330), and lowered TUNEL-positive cell death by 61.8% (p = 0.0015). Tacrolimus achieved hepatoprotection comparable to 12/15-LOX inhibition, but without hepatotoxicity, whereas combined treatment conferred no additional benefit yet bore toxic properties. Conclusions: Tacrolimus preconditioning mitigates hepatic IRI through a glutathione-linked redox–signaling–cell death axis and exerts cytoprotective effects beyond immunosuppression. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress in Ischemia/Reperfusion Injury)
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15 pages, 829 KB  
Article
Redox State of Glutathione and Cysteine in Plasma Following Acute Stroke
by Christopher McGinley, Oyinkansola Adeyemi, Oluwafayokemi Oyolola, Byron D. Ford and Gregory D. Ford
Antioxidants 2026, 15(1), 117; https://doi.org/10.3390/antiox15010117 - 16 Jan 2026
Cited by 1 | Viewed by 1494
Abstract
Ischemic stroke is a major cause of long-term disability and death, with oxidative stress contributing substantially to post-ischemic injury. Reperfusion restores oxygen supply but simultaneously increases reactive oxygen species (ROS), amplifying secondary neuronal damage. This study examined time-dependent changes in systemic thiol redox [...] Read more.
Ischemic stroke is a major cause of long-term disability and death, with oxidative stress contributing substantially to post-ischemic injury. Reperfusion restores oxygen supply but simultaneously increases reactive oxygen species (ROS), amplifying secondary neuronal damage. This study examined time-dependent changes in systemic thiol redox status following transient middle cerebral artery occlusion (tMCAO) in rats. Plasma concentrations of cysteine (CySH), cystine (CySS), glutathione (GSH), and glutathione disulfide (GSSG), along with corresponding CySS/CySH and GSSG/GSH ratios and redox potentials (Eh), were evaluated 24 and 48 h after occlusion. At 24 h, thiol concentrations and redox ratios showed no significant differences between sham and tMCAO groups. By 48 h, a marked oxidative shift emerged, characterized by reduced CySH, elevated GSSG, and significant increases in both CySS/CySH and GSSG/GSH ratios. Redox potentials also demonstrated substantial oxidation at this time point. These findings indicate that prolonged ischemia–reperfusion induces systemic oxidative stress, with plasma redox status serving as a sensitive indicator of reperfusion-related injury. The results underscore the plasma redox status as a potentially sensitive biomarker of reperfusion-induced oxidative injury and support the therapeutic value of targeting redox imbalance to mitigate oxidative damage following stroke. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress in Ischemia/Reperfusion Injury)
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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 - 24 Oct 2025
Cited by 1 | Viewed by 2213
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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