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New Insights in Cardiac Ischemic Diseases

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: closed (31 January 2023) | Viewed by 2860

Special Issue Editors


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Guest Editor
1. Univ-Lyon, CarMeN Laboratory, INSERM 1060, INRA 1397, Université Claude Bernard Lyon1, INSA Lyon, Oullins, France
2. IHU OPERA, Groupement Hospitalier EST, Bâtiment B13, 59 boulevard Pinel, F-69500 Bron, France
Interests: ischemia-reperfusion; post-translational modification; cardiac metabolism

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Co-Guest Editor
Laboratoire HP2, Grenoble Alpes University, INSERM, CHU Grenoble Alpes, 38000 Grenoble, France
Interests: intermittent hypoxia; hypoxia inducible factor-1; myocardial ischemia-reperfusion, metabolism, signaling mathway
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Special Issue Information

Dear Colleagues, 

Cardiac ischemic diseases are the most common causes of death worldwide. Ischemia-Reperfusion (I/R) process leads to O2, metabolic and redox homeostasis alterations inducing tissue critical damages and/or contributing to the remodeling process as well as cardiac function alteration. Indeed, I/R triggers acute or chronic deleterious processes such as oxidative stress, inflammation, sympathetic nervous system activation, endoplasmic reticulum stress, mitochondrial function and dynamic alteration. In recent decades, we have advanced in our understanding of the biological and molecular pathways at the crosstalk of O2 and metabolic homeostasis. More especially, the role of transcriptional activity (i.e., Hypoxia Inducible Factor-1, Nuclear factor-erythroid Factor 2-Related factor 2…) and post-translational modifications (i.e., phosphorylation, acetylation, citrullination, O-GlcNAcylation, Prolyl hydroxylation…) seems to represent innovative targets influencing I/R effects. Nevertheless, pre-clinical or clinical approaches addressing these issues are missing to improve our knowledge to explain deleterious consequences of I/R.

Thus, this Special Issue is dedicated to highlighting new pathways that contribute to the development of cardiac ischemic diseases. We aim to be able to bring a better knowledge for long-term efficient management of the disease. We invite investigators to present recent advances in the comprehension of the molecular pathways leading to acute and chronic response to I/R as well as the development of new approaches to prevent adverse consequences of I/R.

Dr. Delphine Baetz
Dr. Elise Belaïdi
Guest Editors

Manuscript Submission Information

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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

  • cardiac ischemic diseases
  • ischemia-reperfusion
  • cardiac remodeling and function
  • transcriptional activity and post-translational modifications
  • ischemic heart disease
  • heart failure

Published Papers (1 paper)

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Review

19 pages, 1613 KiB  
Review
Tumor Necrosis Factor Family Members and Myocardial Ischemia-Reperfusion Injury: State of the Art and Therapeutic Implications
by Antonella Galeone, Maria Grano and Giacomina Brunetti
Int. J. Mol. Sci. 2023, 24(5), 4606; https://doi.org/10.3390/ijms24054606 - 27 Feb 2023
Cited by 13 | Viewed by 2473
Abstract
Ischemic heart disease is the principal cause of death worldwide and clinically manifests as myocardial infarction (MI), stable angina, and ischemic cardiomyopathy. Myocardial infarction is defined as an irreversible injury due to severe and prolonged myocardial ischemia inducing myocardial cell death. Revascularization is [...] Read more.
Ischemic heart disease is the principal cause of death worldwide and clinically manifests as myocardial infarction (MI), stable angina, and ischemic cardiomyopathy. Myocardial infarction is defined as an irreversible injury due to severe and prolonged myocardial ischemia inducing myocardial cell death. Revascularization is helpful in reducing loss of contractile myocardium and improving clinical outcome. Reperfusion rescues myocardium from cell death but also induces an additional injury called ischemia-reperfusion injury. Multiple mechanisms are involved in ischemia-reperfusion injury, such as oxidative stress, intracellular calcium overload, apoptosis, necroptosis, pyroptosis, and inflammation. Various members of the tumor necrosis factor family play a key role in myocardial ischemia-reperfusion injury. In this article, the role of TNFα, CD95L/CD95, TRAIL, and the RANK/RANKL/OPG axis in the regulation of myocardial tissue damage is reviewed together with their potential use as a therapeutic target. Full article
(This article belongs to the Special Issue New Insights in Cardiac Ischemic Diseases)
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