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New Molecular Insights into Ischemia/Reperfusion: 2nd Edition
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New Molecular Insights into Ischemia/Reperfusion: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 December 2025 | Viewed by 1384

Special Issue Editor

Prof. Dr. Moo-Ho Won

E-Mail Website
Guest Editor
Department of Emergency Medicine, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon 24289, Republic of Korea
Interests: ischemia/reperfusion; neurodegeneration; neurogenesis; cerebral ischemia; aging in CNS
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ischemia/reperfusion (IR) causes a complex pathophysiological process, called IR injury, defined as the paradoxical exacerbation of cellular dysfunction and death following the restoration of blood flow to previously ischemic tissues. IR injury happens in a wide range of organs, including the heart, brain, spinal cord, gut, kidney, and skeletal muscle. IR injury not only involves the ischemic organ itself but also induces systemic damage to distant organs. Huge efforts have been made to develop potential treatments for IR injury, but the molecular and cellular mechanisms of IR injury are not fully understood regarding organs. Therefore, many researchers have been investigating the mechanisms of IR injury in diverse organs using various experimental animal models of IR injury (i.e., different methods of the occlusion of blood vessels and different periods of occlusion time). Principally, the mechanisms of IR injury include excitotoxicity, oxidative stress, and inflammation. Nevertheless, the mechanisms are significantly different depending on the organs. For instance, blood–brain (spinal cord) barrier damage is one of the mechanisms of IR injury in the central nervous system. Therefore, investigation into the molecular mechanisms of IR injury in various organs is warranted so that we can treat or protect against IR injury. Thus, this Special Issue will focus ischemia/reperfusion in various organs, including the heart, brain, spinal cord, liver, and kidneys.

Prof. Dr. Moo-Ho Won
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • vital organs
  • ischemic injury
  • cell and organ dysfunction
  • oxidative stress
  • inflammation
  • excitotoxicity

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Related Special Issue

Published Papers (2 papers)

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10 pages, 2454 KiB  
Article
Glibenclamide Serves as a Potent Vasopressor to Treat Vasoplegia After Cardiopulmonary Bypass and Reperfusion in a Porcine Model
by Andreas Winter, Pascal Nepper, Marcus Hermann, Franziska Bayer, Stephanie Riess, Razan Salem, Jan Hlavicka, Anatol Prinzing, Florian Hecker, Tomas Holubec, Kai Zacharowski, Thomas Walther and Fabian Emrich
Int. J. Mol. Sci. 2025, 26(9), 4040; https://doi.org/10.3390/ijms26094040 - 24 Apr 2025
Viewed by 404
Abstract
The hemodynamic stabilization of patients after complex cardiac surgery is a daily challenge. The use of high doses of catecholamines is common but has potential adverse effects. Glibenclamide, a KATP blocker, seems to attenuate vasoplegia in different animal models of septic shock. [...] Read more.
The hemodynamic stabilization of patients after complex cardiac surgery is a daily challenge. The use of high doses of catecholamines is common but has potential adverse effects. Glibenclamide, a KATP blocker, seems to attenuate vasoplegia in different animal models of septic shock. Therefore, the aim of this study was to investigate the impact of Glibenclamide on the vasoplegic syndrome after cardiopulmonary bypass in a porcine model. In this experimental study, 20 landrace pigs were randomized into two groups and examined: In the control group, standard medical therapy, including norepinephrine, was used, and in the study group standard medical therapy plus additional Glibenclamide was administered. Following general anesthesia, prolonged cardiopulmonary bypass and aortic cross-clamping was performed. In the study group, Glibenclamide was administered 45 min after weaning from cardiopulmonary bypass. The dosage used was 10 mg/kg as a bolus, followed by a continuous infusion of 10 mg/kg/h. Hemodynamic and laboratory measurements were performed. Glibenclamide had a relevant effect on circulatory parameters. With increasing vascular resistance and blood pressure, norepinephrine was able to be reduced. While the heart rate dropped to physiological levels, the cardiac index decreased as well. The results lead to the conclusion that Glibenclamide was able to break through vasoplegic syndrome and could therefore serve as a potent drug to stabilize patients after cardiac surgery. Full article
(This article belongs to the Special Issue New Molecular Insights into Ischemia/Reperfusion: 2nd Edition)
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Review

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16 pages, 1400 KiB  
Review
Factors Contributing to Resistance to Ischemia-Reperfusion Injury in Olfactory Mitral Cells
by Choong-Hyun Lee, Ji Hyeon Ahn and Moo-Ho Won
Int. J. Mol. Sci. 2025, 26(11), 5079; https://doi.org/10.3390/ijms26115079 - 25 May 2025
Viewed by 580
Abstract
Brain ischemia-reperfusion (IR) injury is a critical pathological process that leads to extensive neuronal death, with hippocampal pyramidal cells, particularly those in the cornu Ammonis 1 (CA1) subfield, being highly vulnerable. Until now, human olfactory mitral cell resistance to IR injury has not [...] Read more.
Brain ischemia-reperfusion (IR) injury is a critical pathological process that leads to extensive neuronal death, with hippocampal pyramidal cells, particularly those in the cornu Ammonis 1 (CA1) subfield, being highly vulnerable. Until now, human olfactory mitral cell resistance to IR injury has not been directly studied, but olfactory dysfunction in humans is frequently reported in systemic vascular conditions such as ischemic heart failure and may serve as an early clinical marker of neurological or cardiovascular disease. Mitral cells, the principal neurons of the olfactory bulb (OB), exhibit remarkable resistance to IR injury, suggesting the presence of unique molecular adaptations that support their survival under ischemic stress. Several factors may contribute to the resilience of mitral cells. They have a lower susceptibility to excitotoxicity, mitigating the harmful effects of excessive glutamate signaling. Additionally, they maintain efficient calcium homeostasis, preventing calcium overload—a major trigger for cell death in vulnerable neurons. Mitral cells may also express high baseline levels of antioxidant enzymes and their activities, counteracting oxidative stress. Their robust mitochondrial function enhances energy production and reduces susceptibility to metabolic failure. Furthermore, neuroprotective signaling pathways, including phosphatidylinositol-3-kinase (PI3K)/Akt, mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), and nuclear factor erythroid-2-related factor 2 (Nrf2)-mediated antioxidative responses, further bolster their resistance. In addition to these intrinsic mechanisms, the unique microvascular architecture and metabolic support within the olfactory bulb provide an extra layer of protection. By comparing mitral cells to ischemia-sensitive neurons, key vulnerabilities—such as oxidative stress, excitotoxicity, calcium dysregulation, and mitochondrial dysfunction—can be identified and potentially mitigated in other brain regions. Understanding these molecular determinants of neuronal survival may offer valuable insights for developing novel neuroprotective strategies to combat IR injury in highly vulnerable areas, such as the hippocampus and cortex. Full article
(This article belongs to the Special Issue New Molecular Insights into Ischemia/Reperfusion: 2nd Edition)
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