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Antioxidants
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New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in...
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New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition

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 July 2025 | Viewed by 6667

Special Issue Editors

Dr. Borja Herrero de la Parte

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Guest Editor
Department of Surgery, Faculty of Medicine, Complutense University of Madrid (UCM), 28040 Madrid, Spain
Interests: liver regeneration; liver metastasis; magnetic hyperthermia; nanoparticles; ischemia-reperfusion injury; antioxidants therapy; experimental surgery
Special Issues, Collections and Topics in MDPI journals
Dr. Ignacio García-Alonso

E-Mail Website
Guest Editor
Department of Surgery, Radiology and Physical Medicine, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), 48940 Leioa, Spain
Interests: liver regeneration; liver metastasis; magnetic hyperthermia; nanoparticles; ischemia-reperfusion injury; antioxidants therapy; experimental surgery
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Ana Alonso-Varona

E-Mail Website
Guest Editor
Department of Cell Biology and Histology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), 48940 Leioa, Spain
Interests: tissue engineering; regenerative medicine; oxidative stress; ischemia-reperfusion injury; antioxidants therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleague,

Ischemia–reperfusion injury (IRI) is a critical condition resulting from the sudden loss and subsequent restoration of blood supply to an organ or tissue, leading to significant cellular and tissue damage. This injury occurs due to a lack of oxygen and essential nutrients during ischemia, causing direct cellular harm through decreased ATP and pH levels and increased calcium. Upon reperfusion, the damage is exacerbated by the generation of reactive oxygen species (ROS), inflammatory cytokines, leukocyte recruitment, complement system activation, and changes in capillary permeability. IRI is associated with various clinical scenarios, including cardiovascular surgeries, organ transplants, orthopedic procedures, and conditions like vascular spasms or thromboembolism. It affects multiple organs, such as the heart, retina, and intestines, and is implicated in long-term neurological damage in newborns suffering from perinatal hypoxia.

The Special Issue "New Strategies in Preventing Inflammatory and/or Oxidative-Stress-Induced Damages in Ischemia–Reperfusion Injury, 2nd Edition" builds on the fruitful first edition, which is available at https://www.mdpi.com/si/155268.

Continuing our commitment to advancing IRI research, this edition aims to gather the latest developments in therapies designed to reduce or prevent ischemia–reperfusion injury across various organs and systems. We invite contributions that investigate the application of natural and synthetic antioxidants, stem cells, and their derivatives (such as secretome) as therapeutic strategies.

Submissions may include original research and comprehensive reviews that address (i) a better understanding of the underlying molecular processes involved in IRI; (ii) the progress and current status of the therapeutic management of IRI; and (iii) aspects related to the preservation of the organ function, due to their special clinical interest.

Dr. Borja Herrero de la Parte
Dr. Ignacio García-Alonso
Prof. Dr. Ana Alonso-Varona
Guest Editors

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 100 words) can be sent to the Editorial Office for announcement on this website.

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
  • hypoxia
  • antioxidants
  • therapeutic management

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Published Papers (6 papers)

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Research

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17 pages, 8218 KiB  
Article
The Inhibition of Prolyl Endopeptidase (PREP) by KYP-2047 Treatment to Reduce Myocardial Ischemia/Reperfusion Injury
by Laura Cucinotta, Nicoletta Palermo, Alessio Ardizzone, Anna Paola Capra, Michela Campolo, Emanuela Esposito, Giovanna Casili and Marika Lanza
Antioxidants 2025, 14(4), 442; https://doi.org/10.3390/antiox14040442 - 8 Apr 2025
Viewed by 427
Abstract
Myocardial ischemia–reperfusion injury (MI/R) is a negative and adverse cardiovascular outcome following myocardial ischemia, cardiac surgery, or circulatory arrest. Prolyl endopeptidase (PREP) appears to be involved in inflammatory responses, so it could be a possible therapeutic target for counteracting ischemia injury. This study [...] Read more.
Myocardial ischemia–reperfusion injury (MI/R) is a negative and adverse cardiovascular outcome following myocardial ischemia, cardiac surgery, or circulatory arrest. Prolyl endopeptidase (PREP) appears to be involved in inflammatory responses, so it could be a possible therapeutic target for counteracting ischemia injury. This study aimed to investigate the role of PREP inhibitor, KYP-2047 (4-phenylbutanoyl-l-prolyl-2(S)-cyanopyrolidine), in the modulation of molecular and biochemical processes involved in MI/R. MI/R was induced through coronary artery occlusion (15 min), followed by reperfusion (2 h). KYP-2047 was intraperitoneally administrated at doses of 2.5 mg/kg and 5 mg/kg 24 h before the surgical procedures. The hearts were removed and processed for analysis. KYP-2047 treatment limited ischemic myocardial-induced histological damage and neutrophil accumulation, limiting inflammation, fibrosis, and apoptosis processes. Additionally, KYP-2047 was able to modulate p-38 and p-ERK expression, suggesting an improving role in recovering cardiac function. These findings highlighted the protective effects of KYP-2047 pretreatment in MI/R injury, suggesting PREP as a potential target therapy for the pathogenesis of MI/R. Although the molecular mechanisms underlying the action of KYP-2047 are still to be explored, these results suggested that the regulation of NF-κB, apoptosis, and MAPK pathways by KYP-2047 treatment could preventatively limit the damage caused by MI/R. Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition)
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13 pages, 3805 KiB  
Article
Intermittent Fasting Protects Against the Progression from Acute Kidney Injury to Chronic Kidney Disease
by Yoonjoo Jang, Young Suk Kim, Seo Rin Kim, Dong Won Lee, Soo Bong Lee and Il Young Kim
Antioxidants 2025, 14(1), 119; https://doi.org/10.3390/antiox14010119 - 20 Jan 2025
Viewed by 2058
Abstract
Acute kidney injury (AKI) is a major but often underestimated risk factor for the development of chronic kidney disease (CKD). Exploring innovative approaches to prevent this progression is critical. Intermittent fasting (IF), recognized for its metabolic and anti-inflammatory benefits, may offer protective effects [...] Read more.
Acute kidney injury (AKI) is a major but often underestimated risk factor for the development of chronic kidney disease (CKD). Exploring innovative approaches to prevent this progression is critical. Intermittent fasting (IF), recognized for its metabolic and anti-inflammatory benefits, may offer protective effects in this context. Using a unilateral ischemia-reperfusion injury (UIRI) model in male C57BL/6 mice, we evaluated the impact of IF on tubulointerstitial fibrosis and tubular epithelial–mesenchymal transition (EMT) over 8 weeks. Mice in the IF group followed a 5:2 regimen, fasting for 24 h twice weekly. Four groups were studied: control, IF, UIRI, and IF + UIRI. The UIRI group exhibited increased fibrosis and EMT, both of which were significantly attenuated in the IF + UIRI group. IF also reduced levels of TGF-β1, phosphorylated NF-κB p65, inflammatory cytokines, and F4/80-positive macrophages, along with markers of oxidative stress. These findings highlight IF’s ability to mitigate fibrosis and EMT through reductions in inflammation and oxidative stress during AKI-to-CKD progression. Our study suggests that IF may serve as a promising dietary strategy to prevent AKI from advancing into CKD. Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition)
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15 pages, 4169 KiB  
Article
Exercise-Intervened Circulating Extracellular Vesicles Alleviate Oxidative Stress in Cerebral Microvascular Endothelial Cells Under Hypertensive Plus Hypoxic Conditions
by Smara Sigdel, Shuzhen Chen, Gideon Udoh and Jinju Wang
Antioxidants 2025, 14(1), 77; https://doi.org/10.3390/antiox14010077 - 10 Jan 2025
Viewed by 820
Abstract
Our group has recently demonstrated that exercise intervention affects the release and function of bone marrow endothelial progenitor cell-derived extracellular vesicles (EVs) in transgenic hypertensive mice. Whether such an exercise regimen can impact circulating EVs (cEVs) remains unknown. In this study, we investigated [...] Read more.
Our group has recently demonstrated that exercise intervention affects the release and function of bone marrow endothelial progenitor cell-derived extracellular vesicles (EVs) in transgenic hypertensive mice. Whether such an exercise regimen can impact circulating EVs (cEVs) remains unknown. In this study, we investigated the influence of exercise on cEV level and function. Transgenic hypertensive mice (Alb1-Ren) underwent 8-week treadmill exercise (10 m/min for 1 h, 5 days per week). Age- and sex-matched sedentary Alb1-Ren mice served as controls. cEVs were isolated from the blood of exercised and sedentary mice and are denoted as ET-cEV and nET-cEV, respectively. cEVs were labeled to determine their uptake efficiency and pathways. The functions of cEVs were assessed in an Angiotensin II (Ang II) plus hypoxia-injured cerebral microvascular endothelial cell (mBMEC) injury model. Cellular migration ability and oxidative stress were evaluated. We found that treadmill exercise stimulated cEV release, and ET-cEVs were more prone to be internalized by mBMECs. The ET-cEV internalization was mediated by macropinocytosis and endocytosis pathways. Functional studies showed that ET-cEVs can improve the compromised migration capability of mBMECs challenged by Ang II plus hypoxia. Additionally, ET-cEV treatment upregulated the expression of p-Akt/Akt in mBMECs. Compared to nET-cEVs, ET-cEVs significantly reduced ROS overproduction in Ang II plus hypoxia-injured mBMECs, associated with decreased Nox2 expression. All these findings suggest that exercise-intervened cEVs can protect cerebral microvascular endothelial cells against hypertensive and hypoxic injury. Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition)
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19 pages, 4303 KiB  
Article
Restoration of Sestrin 3 Expression Mitigates Cardiac Oxidative Damage in Ischemia–Reperfusion Injury Model
by Mina Park, Sunghye Cho and Dongtak Jeong
Antioxidants 2025, 14(1), 61; https://doi.org/10.3390/antiox14010061 - 7 Jan 2025
Viewed by 811
Abstract
Cardiac ischemia–reperfusion injury (IRI) occurs when blood flow is restored to the myocardium after a period of ischemia, leading to oxidative stress and subsequent myocardial cell damage, primarily due to the accumulation of reactive oxygen species (ROS). In our previous research, we identified [...] Read more.
Cardiac ischemia–reperfusion injury (IRI) occurs when blood flow is restored to the myocardium after a period of ischemia, leading to oxidative stress and subsequent myocardial cell damage, primarily due to the accumulation of reactive oxygen species (ROS). In our previous research, we identified that miR-25 is significantly overexpressed in pressure overload-induced heart failure, and its inhibition improves cardiac function by restoring the expression of SERCA2a, a key protein involved in calcium regulation. In this study, we aimed to investigate the role of miR-25 in the context of ischemia–reperfusion injury. We found that miR-25 was markedly upregulated under hypoxic conditions in both in vitro and in vivo models. Through in silico analysis, we identified Sestrin3 (SESN3), an antioxidant protein known for its protective effects against oxidative stress, as a novel target of miR-25. Based on these findings, we hypothesized that inhibiting miR-25 would restore Sestrin3 expression, thereby reducing ROS-induced myocardial cell damage and improving cardiac function. To test this hypothesis, we employed two model systems: a hypoxia/reoxygenation (H/R) stress model using H9c2 myoblasts and a surgically induced ischemia–reperfusion injury mouse model. Our results demonstrated that the use of miR-25 inhibitors significantly improved cardiac function and reduced myocardial damage in both models through the restoration of SESN3 expression. In conclusion, our findings suggest that targeting miR-25 may serve as a novel therapeutic modality to alleviate oxidative damage in the heart. Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition)
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Review

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16 pages, 705 KiB  
Review
Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia–Reperfusion Injury
by Naranjan S. Dhalla, Petr Ostadal and Paramjit S. Tappia
Antioxidants 2025, 14(3), 340; https://doi.org/10.3390/antiox14030340 - 14 Mar 2025
Viewed by 635
Abstract
Delayed reperfusion of the ischemic heart (I/R) is known to impair the recovery of cardiac function and produce a wide variety of myocardial defects, including ultrastructural damage, metabolic alterations, subcellular Ca2+-handling abnormalities, activation of proteases, and changes in cardiac gene expression. [...] Read more.
Delayed reperfusion of the ischemic heart (I/R) is known to impair the recovery of cardiac function and produce a wide variety of myocardial defects, including ultrastructural damage, metabolic alterations, subcellular Ca2+-handling abnormalities, activation of proteases, and changes in cardiac gene expression. Although I/R injury has been reported to induce the formation of reactive oxygen species (ROS), inflammation, and intracellular Ca2+ overload, the generation of oxidative stress is considered to play a critical role in the development of cardiac dysfunction. Increases in the production of superoxide, hydroxyl radicals, and oxidants, such as hydrogen peroxide and hypochlorous acid, occur in hearts subjected to I/R injury. In fact, mitochondria are a major source of the excessive production of ROS in I/R hearts due to impairment in the electron transport system as well as activation of xanthine oxidase and NADPH oxidase. Nitric oxide synthase, mainly present in the endothelium, is also activated due to I/R injury, leading to the production of nitric oxide, which, upon combination with superoxide radicals, generates nitrosative stress. Alterations in cardiac function, sarcolemma, sarcoplasmic reticulum Ca2+-handling activities, mitochondrial oxidative phosphorylation, and protease activation due to I/R injury are simulated upon exposing the heart to the oxyradical-generating system (xanthine plus xanthine oxidase) or H2O2. On the other hand, the activation of endogenous antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, and the concentration of a transcription factor (Nrf2), which modulates the expression of various endogenous antioxidants, is depressed due to I/R injury in hearts. Furthermore, pretreatment of hearts with antioxidants such as catalase plus superoxide dismutase, N-acetylcysteine, and mercaptopropionylglycerine has been observed to attenuate I/R-induced subcellular Ca2+ handling and changes in Ca2+-regulatory activities; additionally, it has been found to depress protease activation and improve the recovery of cardiac function. These observations indicate that oxidative stress is intimately involved in the pathological effects of I/R injury and different antioxidants attenuate I/R-induced subcellular alterations and improve the recovery of cardiac function. Thus, we are faced with the task of developing safe and effective antioxidants as well as agents for upregulating the expression of endogenous antioxidants for the therapy of I/R injury. Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition)
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22 pages, 1799 KiB  
Review
Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
by Dario Troise, Costanza Allegra, Luciana Antonia Cirolla, Silvia Mercuri, Barbara Infante, Giuseppe Castellano and Giovanni Stallone
Antioxidants 2025, 14(1), 66; https://doi.org/10.3390/antiox14010066 - 8 Jan 2025
Viewed by 1159
Abstract
The complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia–reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft function. Complement activation, [...] Read more.
The complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia–reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft function. Complement activation, particularly the alternative pathway, participates in the pathogenesis of IRI, involving all kidney compartments. In particular, tubular epithelial cells often acquire a dysfunctional phenotype that can exacerbate complement activation and kidney damage. Currently, complement-modulating drugs are under investigation for the treatment of kidney diseases. Many of these drugs have shown potential therapeutic benefits, but no effective clinical treatments for renal IRI have been identified yet. In this review, we will explore drugs that target complement factors, complement receptors, and regulatory proteins, aiming to highlight their potential value in improving the management of renal IRI. Full article
(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative Stress-Induced Damages in Ischemia-Reperfusion Injury, 2nd Edition)
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