Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms.

Autor:	Maslov LN; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Popov SV; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Mukhomedzyanov AV; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Naryzhnaya NV; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Voronkov NS; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Ryabov VV; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Boshchenko AA; Laboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia., Khaliulin I; School of Clinical Sciences, University of Bristol, Bristol Royal Infirmary, Bristol, UK., Prasad NR; Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamilnadu, India., Fu F; Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, Xi\'an, China., Pei JM; Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, Xi\'an, China., Logvinov SV; Department of Histology, Embryology and Cytology, Siberian State Medical University, 634055 Tomsk, Russia., Oeltgen PR; Department of Pathology, University of Kentucky College of Medicine, Lexington, KY, USA.
Jazyk:	angličtina
Zdroj:	Current cardiology reviews [Curr Cardiol Rev] 2022; Vol. 18 (5), pp. 63-79.
DOI:	10.2174/1573403X18666220413121730
Abstrakt:	It has been documented that Ca 2+ 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. (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
Databáze:	MEDLINE
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