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Current Cardiology Reviews

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ISSN (Print): 1573-403X
ISSN (Online): 1875-6557

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Review Article

Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms

Author(s): Leonid N. Maslov*, Sergey V. Popov, Alexandr V. Mukhomedzyanov, Natalia V. Naryzhnaya, Nikita S. Voronkov, Vyacheslav V. Ryabov, Alla A. Boshchenko, Igor Khaliulin, N. Rajendra Prasad, Feng Fu, Jian-Ming Pei, Sergey V. Logvinov and Peter R. Oeltgen

Volume 18, Issue 5, 2022

Published on: 14 June, 2022

Article ID: e130422203525 Pages: 17

DOI: 10.2174/1573403X18666220413121730

Price: $65

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.

Keywords: Heart, reperfusion injury, Ca2+ overload, oxidative stress, inflammation, apoptosis.

Graphical Abstract

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