IMR Press / FBS / Volume 13 / Issue 2 / DOI: 10.52586/S556
Open Access Review
Mitochondrial mechanisms by which gasotransmitters (H2S, NO and CO) protect cardiovascular system against hypoxia
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1 Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 194223 Saint-Petersburg, Russian
2 Advocate Aurora Health Care, Advocate Aurora Research Institute, Milwaukee, WI 53215, USA
*Correspondence: (Irina Shemarova)
Front. Biosci. (Schol Ed) 2021, 13(2), 105–130;
Submitted: 27 February 2021 | Revised: 9 May 2021 | Accepted: 12 May 2021 | Published: 3 December 2021
Copyright: © 2021 The Author(s). Published by BRI.
This is an open access article under the CC BY 4.0 license (

Over past few years, there has been a dramatic increase in studying physiological mechanisms of the activity of various signaling low-molecular molecules that directly or indirectly initiate adaptive changes in the cardiovascular system cells (CVSC) to hypoxia. These molecules include biologically active endogenous gases or gasotransmitters (H2S, NO and CO) that influence on many cellular processes, including mitochondrial biogenesis, oxidative phosphorylation, K+/Ca2+ exchange, contractility of cardiomyocytes (CM) and vascular smooth muscle cells (VSMC) under conditions of oxygen deficiency. The present review focuses on the mechanistic role of the gasotransmitters (NO, H2S, CO) in cardioprotection. The structural components of these mechanisms involve mitochondrial enzyme complexes and redox signal proteins, K+ and Ca2+ channels, and mitochondrial permeability transition pore (MPTP) that have been considered as the final molecular targets of mechanisms underlying antioxidant and mild mitochondrial uncoupling effects, preconditioning, vasodilatation and adaptation to hypoxia. In this article, we have reviewed recent findings on the gasotransmitters and proposed a unifying model of mitochondrial mechanisms of cardioprotection.

Carbon monoxide
Hydrogen sulfide
Ionic channels
Nitric oxide
Fig. 1.
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