Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms-Reference-Cited by-同舟云学术

Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms

Published:2022-09 Issue:5 Volume:18 Page:
ISSN:1573-403X
Container-title:Current Cardiology Reviews
language:en
Short-container-title:CCR

Author:

Maslov Leonid N.¹,Popov Sergey V.¹,Mukhomedzyanov Alexandr V.¹,Naryzhnaya Natalia V.¹,Voronkov Nikita S.¹,Ryabov Vyacheslav V.¹,Boshchenko Alla A.¹,Khaliulin Igor²,Prasad N. Rajendra³,Fu Feng⁴,Pei Jian-Ming⁴,Logvinov Sergey V.⁵,Oeltgen Peter R.⁶

Affiliation:

1. Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia

2. School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, UK

3. Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamilnadu, India

4. Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, Xi\'an, China

5. Department of Histology, Embryology and Cytology, Siberian State Medical University, 634055 Tomsk, Russia

6. Department of Pathology, University of Kentucky College of Medicine, Lexington, KY, USA

Abstract

Abstract:It has been documented that Ca2+ overload and increased production of reactive oxygen species play a significant role in reperfusion injury (RI) of cardiomyocytes. Ischemia/reperfusion induces cell death as a result of necrosis, necroptosis, apoptosis, and possibly autophagy, pyroptosis and ferroptosis. It has also been demonstrated that the NLRP3 inflammasome is involved in RI of the heart. An increase in adrenergic system activity during the restoration of coronary perfusion negatively affected cardiac resistance to RI. Toll-like receptors are involved in RI of the heart. Angiotensin II and endothelin-1 aggravated ischemic/reperfusion injury of the heart. Activation of neutrophils, monocytes, CD4+ T-cells and platelets contributes to cardiac ischemia/reperfusion injury. Our review outlines the role of these factors in reperfusion cardiac injury.

Funder

Russian Foundation of Basic Research

National Natural Science Foundation of China

Publisher

Bentham Science Publishers Ltd.

Subject

Cardiology and Cardiovascular Medicine,General Medicine

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