Advanced Research in Reperfusion of Cardiac 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 (31 October 2023) | Viewed by 3460

Special Issue Editor


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Guest Editor
Cardiology Research Institute, Tomsk National Research Medical Center, the Russian Academy of Sciences, 111A Kievskaya Str., Tomsk, Russia
Interests: ischemic and reperfusion heart damage; opioid receptor; conditioning; high altitude hypoxia; NO-syntase; kinases; mitochondria

Special Issue Information

Dear Colleagues,

It is generally accepted that only the restoration of coronary blood flow can affect infarct size. However, reperfusion injury (RI) is responsible for up to 50% of final infarct size. Many factors are involved in cell death during reperfusion, among which the most important are reactive oxygen species production, Ca2+ overload, and inflammation. In recent decades, many pathways of regulated cell death have been investigated. Reperfusion induces cell death as a result of necrosis, necroptosis, apoptosis, pyroptosis, ferroptosis and possibly autophagy. It has also been demonstrated that the NLRP3 inflammasome is involved in RI of the heart. Unfortunately, there are no drugs that could effectively prevent reperfusion injury that occurs after restoration of coronary perfusion in patients with acute myocardial infarction. Studies of the mechanisms of reperfusion injury can be used for search of pharmacological targets for protecting the myocardium against RI.

Therefore, the aim of this Special Issue of Biomedicines entitled “Advanced Research in Reperfusion of Cardiac Injury” is an overview of the current state of research, promoting new understanding of the mechanisms of RI, and considering possible approaches to correct RI.

Both original articles and reviews consistent with this research topic will be considered for publication in this Special Issue. Both original articles and reviews will be considered for publishing in this Special Issue.

Dr. Natalia V. Naryzhnaya
Guest Editor

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Keywords

  • reperfusion
  • cell death pathways
  • cardiac protection
  • myocardial conditioning

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Published Papers (2 papers)

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Research

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17 pages, 1160 KiB  
Article
Role of Angiopoietic Coronary Endothelial Dysfunction in the Pathogenesis of Ischemic Cardiomyopathy
by Svetlana P. Chumakova, Olga I. Urazova, Vladimir M. Shipulin, Sergey L. Andreev, Olga A. Denisenko, Margarita V. Gladkovskaya, Larisa S. Litvinova and Mikhail A. Bubenchikov
Biomedicines 2023, 11(7), 1950; https://doi.org/10.3390/biomedicines11071950 - 10 Jul 2023
Cited by 1 | Viewed by 1336
Abstract
Background: The angiopoietic endothelial dysfunction in ischemic cardiomyopathy (ICMP) remains unexplored. Aim: The identification of the imbalance of endothelial dysfunction mediators and the number of endothelial progenitor (EPC) and desquamated (EDC) cells in patients with coronary heart disease (CHD) with and without ICMP. [...] Read more.
Background: The angiopoietic endothelial dysfunction in ischemic cardiomyopathy (ICMP) remains unexplored. Aim: The identification of the imbalance of endothelial dysfunction mediators and the number of endothelial progenitor (EPC) and desquamated (EDC) cells in patients with coronary heart disease (CHD) with and without ICMP. Methods: A total of 87 patients (47 with ICMP and 40 without ICMP) were observed. The content of EPCs (CD14+CD34+VEGFR2+) in vein blood and EDCs (CD45CD146+) in the blood from the coronary sinus and cubital vein was determined by flow cytometry. The contents of HIF-1α and HIF-2α in vein blood as well as that of ADMA and endothelin-1 in sinus plasma and angiopoietin-2, MMP-9 and galectin-3 in both samples were assessed using ELISA, and VEGF, PDGF, SDF-1 and MCP-1 contents using immunofluorescence. Results: ADMA and endothelin-1 levels in the sinus blood were comparable between the patient groups; a deficiency of HIF-1α and excess of HIF-2α were detected in the vein blood of ICMP patients. The EDC content in the vein blood increased in CHD patients regardless of ICMP, and the concentrations of VEGF-A, VEGF-B, PDGF, MCP-1, angiopoietin-2, and MMP-9 were normal. In ICMP patients, vein blood was characterized by an excess of galectin-3 and sinus blood by an excess of EDCs, angiopoietin-2, MMP-9 and galectin-3. Conclusion: ICMP is accompanied by angiopoietic endothelial dysfunction. Full article
(This article belongs to the Special Issue Advanced Research in Reperfusion of Cardiac Injury)
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Review

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12 pages, 676 KiB  
Review
δ-Opioid Receptor as a Molecular Target for Increasing Cardiac Resistance to Reperfusion in Drug Development
by Natalia V. Naryzhnaya, Alexander V. Mukhomedzyanov, Maria Sirotina, Leonid N. Maslov, Boris K. Kurbatov, Alexander S. Gorbunov, Mikhail Kilin, Artur Kan, Andrey V. Krylatov, Yuri K. Podoksenov and Sergey V. Logvinov
Biomedicines 2023, 11(7), 1887; https://doi.org/10.3390/biomedicines11071887 - 3 Jul 2023
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Abstract
An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ2-opioid receptor (δ2-OR) increases the cardiac tolerance to reperfusion. It has been found that this δ2-OR is localized [...] Read more.
An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ2-opioid receptor (δ2-OR) increases the cardiac tolerance to reperfusion. It has been found that this δ2-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion. The infarct-limiting effect of the δ2-OR agonist deltorphin II depends on the activation of several protein kinases, including PKCδ, ERK1/2, PI3K, and PKG. Hypothetical end-effectors of the cardioprotective effect of deltorphin II are the sarcolemmal KATP channels and the MPT pore. Full article
(This article belongs to the Special Issue Advanced Research in Reperfusion of Cardiac Injury)
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