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Biomedicines
Special Issues
Molecular Mechanism of Ischemia and Reperfusion Injury
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Molecular Mechanism of Ischemia and Reperfusion Injury

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 10225

Special Issue Editors

Prof. Dr. Rosanna Di Paola

E-Mail Website
Guest Editor
Department of Veterinary Sciences, University of Messina, Viale SS Annunziata, 98168 Messina, Italy
Interests: biochemistry; diet; mithocondrial disfunction; animal models; molecular pathways
Special Issues, Collections and Topics in MDPI journals
Dr. Enrico Gugliandolo

E-Mail Website
Guest Editor
Department of Veterinary Science, University of Messina, 98155 Messina, Italy
Interests: veterinary pharmacology; toxicology; pharmacological activity of natural substances; nutraceuticals; dietary contaminants; animal welfare
Special Issues, Collections and Topics in MDPI journals
Dr. Roberta Fusco

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: biochemistry; molecular mechanism; oxidative stress; endometriosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ischemia and reperfusion–elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. The generation of reactive oxygen species (ROS) increases due to a lower concentration of antioxidative agents in ischemic cells. ROS cause oxidative stress that promotes endothelial dysfunction, DNA damage, and local inflammatory responses. Inflammatory cascades and oxidative stress may subsequently induce a cytokine storm, resulting in cell death caused by damage to cellular structures. The reperfusion stage is dynamic and may persist for several days. Understanding the detailed mechanism of ischemia-reperfusion injury may provide a strong foundation not only for novel therapeutic opportunities, but also for injury prevention.

The current Special Issue focuses on molecular and cellular mechanisms underlining pathogenesis and novel therapeutic approaches targeting the ischemia and reperfusion injuries. We welcome research or review articles focusing on the topics.

Prof. Dr. Rosanna Di Paola
Dr. Enrico Gugliandolo
Dr. Roberta Fusco
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. Biomedicines 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 2600 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

  • molecular mechanism
  • biochemistry
  • One Health
  • animals
  • toxicology

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Published Papers (4 papers)

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Research

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5 pages, 5235 KiB  
Communication
Precise Definition of Porcine Hippocampal Cornu Ammonis 2: High Histoarchitectural Similarity to Humans but Unequal Sensitivity to Hypoxia
by Miriam Renz, Pascal Siegert, Katja Mohnke, Robert Ruemmler, Katrin Frauenknecht, Clemens Sommer and Anja Harder
Biomedicines 2024, 12(8), 1896; https://doi.org/10.3390/biomedicines12081896 - 19 Aug 2024
Viewed by 608
Abstract
Experimental animal studies of hypoxic–ischemic injury of the hippocampus of pigs are limited due to the unprecise definition of hippocampal subfields, cornu ammonis 1 to 4, compared to humans. Given that the pig model closely mirrors human physiology and serves as an important [...] Read more.
Experimental animal studies of hypoxic–ischemic injury of the hippocampus of pigs are limited due to the unprecise definition of hippocampal subfields, cornu ammonis 1 to 4, compared to humans. Given that the pig model closely mirrors human physiology and serves as an important model for critical care research, a more precise description is necessary to draw valid conclusions applicable to human diseases. In our study, we were able to precisely define the CA2 and its adjacent regions in a domestic pig model by arginine vasopressin receptor 1B (AVPR1B) and calbindin-D28K like (CaBP-Li) expression patterns. Our findings demonstrate that the histoarchitecture of the porcine cornu ammonis subfields closely resembles that of the human hippocampus. Notably, we identified unusually strong neuronal damage in regions of the pig hippocampus following global ischemia, which are typically not susceptible to hypoxic–ischemic damage in humans. Full article
(This article belongs to the Special Issue Molecular Mechanism of Ischemia and Reperfusion Injury)
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13 pages, 3842 KiB  
Article
The Role of Gut Microbiota and Circadian Rhythm Oscillation of Hepatic Ischemia–Reperfusion Injury in Diabetic Mice
by Juan Li, Yanbo Liu, Yijing Li, Tianning Sun, Hongbing Xiang and Zhigang He
Biomedicines 2024, 12(1), 54; https://doi.org/10.3390/biomedicines12010054 - 25 Dec 2023
Cited by 1 | Viewed by 1502
Abstract
Circadian rhythm oscillation and the gut microbiota play important roles in several physiological functions and pathology regulations. In this study, we aimed to elucidate the characteristics of diabetic hepatic ischemia–reperfusion injury (HIRI) and the role of the intestinal microbiota in diabetic mice with [...] Read more.
Circadian rhythm oscillation and the gut microbiota play important roles in several physiological functions and pathology regulations. In this study, we aimed to elucidate the characteristics of diabetic hepatic ischemia–reperfusion injury (HIRI) and the role of the intestinal microbiota in diabetic mice with HIRI. Hepatic ischemia–reperfusion injury surgery was performed at ZT0 or ZT12. The liver pathological score and the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed to evaluate liver injury. We conducted an FMT experiment to examine the role of intestinal microbiota in diabetic mice with HIRI. The 16S rRNA gene sequencing of fecal samples was performed for microbial analysis. Our results showed that hyperglycemia aggravated HIRI in diabetic mice, but there was no diurnal variation seen in diabetic HIRI. We also demonstrated that there were significant alterations in the gut microbiota composition between the diabetic and control mice and that gut microbiota transplantation from diabetic mice had obvious harmful effects on HIRI. These findings provide some useful information for the future research of diabetic mice with HIRI. Full article
(This article belongs to the Special Issue Molecular Mechanism of Ischemia and Reperfusion Injury)
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Review

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11 pages, 1040 KiB  
Review
The cGAS-STING Pathway: A New Therapeutic Target for Ischemia–Reperfusion Injury in Acute Myocardial Infarction?
by Mengxiang Tian, Fengyuan Li and Haiping Pei
Biomedicines 2024, 12(8), 1728; https://doi.org/10.3390/biomedicines12081728 - 2 Aug 2024
Viewed by 6480
Abstract
The innate immune system is the body’s natural defense system, which recognizes a wide range of microbial molecules (such as bacterial DNA and RNA) and abnormal molecules within cells (such as misplaced DNA, self-antigens) to play its role. DNA released into the cytoplasm [...] Read more.
The innate immune system is the body’s natural defense system, which recognizes a wide range of microbial molecules (such as bacterial DNA and RNA) and abnormal molecules within cells (such as misplaced DNA, self-antigens) to play its role. DNA released into the cytoplasm activates the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling pathway to initiate an immune response. Ischemia–reperfusion injury (IRI) after acute myocardial infarction refers to the phenomenon where myocardial tissue suffers further damage upon the restoration of blood flow. This issue is a significant clinical problem in the treatment of myocardial infarction, as it can diminish the effectiveness of reperfusion therapy and lead to further deterioration of cardiac function. Studies have found that the cGAS-STING signaling pathway is closely related to this phenomenon. Therefore, this review aims to describe the role of the cGAS-STING signaling pathway in ischemia–reperfusion injury after myocardial infarction and summarize the current development status of cGAS-STING pathway inhibitors and the application of nanomaterials to further elucidate the potential of this pathway as a therapeutic target. Full article
(This article belongs to the Special Issue Molecular Mechanism of Ischemia and Reperfusion Injury)
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14 pages, 1782 KiB  
Review
Energy Metabolism and Metformin: Effects on Ischemia-Reperfusion Injury in Kidney Transplantation
by Denise V. Nemeth, Leonardo Iannelli, Elena Gangitano, Vito D’Andrea and Maria Irene Bellini
Biomedicines 2024, 12(7), 1534; https://doi.org/10.3390/biomedicines12071534 - 10 Jul 2024
Viewed by 989
Abstract
Metformin (MTF) is the only biguanide included in the World Health Organization’s list of essential medicines; representing a widespread drug in the management of diabetes mellitus. With its accessibility and affordability being one of its biggest assets, it has become the target of [...] Read more.
Metformin (MTF) is the only biguanide included in the World Health Organization’s list of essential medicines; representing a widespread drug in the management of diabetes mellitus. With its accessibility and affordability being one of its biggest assets, it has become the target of interest for many trying to find alternative treatments for varied pathologies. Over time, an increasing body of evidence has shown additional roles of MTF, with unexpected interactions of benefit in other diseases. Metformin (MTF) holds significant promise in mitigating ischemia-reperfusion injury (IRI), particularly in the realm of organ transplantation. As acceptance criteria for organ transplants expand, IRI during the preservation phase remain a major concern within the transplant community, prompting a keen interest in MTF’s effects. Emerging evidence suggests that administering MTF during reperfusion may activate the reperfusion injury salvage kinase (RISK) pathway. This pathway is pivotal in alleviating IRI in transplant recipients, potentially leading to improved outcomes such as reduced rates of organ rejection. This review aims to contextualize MTF historically, explore its current uses, pharmacokinetics, and pharmacodynamics, and link these aspects to the pathophysiology of IRI to illuminate its potential future role in transplantation. A comprehensive survey of the current literature highlights MTF’s potential to recondition and protect against IRI by attenuating free radical damage, activating AMP-activated protein kinase to preserve cellular energy and promote repair, as well as directly reducing inflammation and enhancing microcirculation. Full article
(This article belongs to the Special Issue Molecular Mechanism of Ischemia and Reperfusion Injury)
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