Mitochondrial mechanisms by which gasotransmitters (H2S, NO and CO) protect cardiovascular system against hypoxia

Authors

Irina Shemarova, Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 194223 Saint-Petersburg, Russian.
Vladimir Nesterov, Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 194223 Saint-Petersburg, Russian.
Larisa Emelyanova, Advocate Aurora Health
Sergey Korotkov, Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 194223 Saint-Petersburg, Russian.

Recommended Citation

Shemarova I, Nesterov V, Emelyanova L, Korotkov S. Mitochondrial mechanisms by which gasotransmitters (H2S, NO and CO) protect cardiovascular system against hypoxia. Front Biosci (Schol Ed). 2021;13(2):105-130. doi:10.52586/S556

Affiliations

Advocate Aurora Research Institute

Abstract

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/Ca 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 Ca 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.

Document Type

Article

PubMed ID

34879465