Abstract
Cardiovascular disease is the main cause of death worldwide, but its pathogenesis is not yet clear. Hydrogen sulfide (H2S) is considered to be the third most important endogenous gasotransmitter in the organism after carbon monoxide and nitric oxide. It can be synthesized in mammalian tissues and can freely cross the cell membrane and exert many biological effects in various systems including cardiovascular system. More and more recent studies have supported the protective effects of endogenous H2S and exogenous H2S-releasing compounds (such as NaHS, Na2S, and GYY4137) in cardiovascular diseases, such as cardiac hypertrophy, heart failure, ischemia/reperfusion injury, and atherosclerosis. Here, we provided an up-to-date overview of the mechanistic actions of H2S as well as the therapeutic potential of various classes of H2S donors in treating cardiovascular diseases.
Highlights
Hydrogen sulfide (H2S) is a colorless, smelly water soluble gas (Wang, 2010)
The most common H2S donors used in biological research are sulfide salts, NaSH and Na2S, which have been proven to release a large amount of gas in a short time and are widely used for evaluating the therapeutic potential of exogenous H2S (Predmore et al, 2012)
For vascular smooth muscle cells (VSMCs) isolated from mesenteric arteries of wild type and cystathionine gamma-lyase (CSE) knockout mice, Insulin-like growth factor-1 (IGF-1) increases the proliferation of VSMCs, and the effect is more pronounced in CSE knockout-VSMCs
Summary
Hydrogen sulfide (H2S) is a colorless, smelly water soluble gas (Wang, 2010). It was first described in the 17th century (Wang, 2012). H2S is considered to be the third most important endogenous gas molecule in the organism after carbon monoxide (CO) and nitric oxide (NO) (Wang, 2002; Hartle and Pluth, 2016; Szabo, 2016) It can be synthesized in mammalian tissues and can freely cross the cell membrane and exert many biological effects in various systems (Wang, 2012). CSE expression was reduced in oxidized LDL (Ox-LDL)-stimulated human aortic endothelial cells (HAEC) and in the aorta of high fat dietinduced ApoE(−/−) mice (Leucker et al, 2017). In mouse and human atherosclerosis, CSE expression is upregulated, but circulating and plaque levels of H2S are reduced, a phenomenon that can be attributed to inhibition of CSE enzyme activity (Bibli et al, 2018). The miRNA induces silencing complex (RISC) to degrade mRNA or hinder translation
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