FIGURE 1.

H₂S in the cardiovascular system. H₂S inhibits the occurrence and development of atherosclerosis by inhibiting the proliferation and migration of VSMCs, relaxing blood vessels, inhibiting inflammation, and inhibiting lipid accumulation and vascular calcification. In addition, H₂S inhibits cardiac remodeling and cardiac ischemia-reperfusion injury by improving energy metabolism, anti-oxidation, anti-apoptosis, angiogenesis, and enhancing autophagy. The notation ↑ indicates increase or activation, and ↓indicates decrease or suppression. Abbreviations: STS, sodium thiosulfate; 4-CPI, 4-carboxyphenyl isothiocyanate; SPRC, S-propargyl-cysteine (also called ZYZ-802), a novel slow release H₂S release compound (FW1256); VSMCs, vascular smooth muscle cells; ACE2, angiotensin converting enzyme 2; IGF-1, insulin-like growth factor-1; ANP, atrial natriuretic peptide; BKCa, large-conductance Ca⁽²⁺⁾-activated potassium channel; Cyp2C, cytochrome P-450 2C; K_ATP, ATP-sensitive potassium channel; ET-1, endothelin-1; Hb, hemoglobin; JMJD3, Jumonji domain protein 3; TNFα, tumor necrosis factor alpha; IL6, interleukin 6′; JNK, c-Jun NH2-terminal kinase; NF-κB, nuclear factor-kappa B; Nox4, NADPH oxidase member NADPH oxidase 4; ROS, reactive oxygen species; Sirt1, sirtuin 1; Sirt3, sirtuin 3; HIF-1α, hypoxia-inducible factor 1-alpha; GSH, glutathione; NRF2, nuclear factor (erythrocyte-derived 2)-like 2; NQO1, NADPH dehydrogenase 1; ABCA1, ATP-binding cassette transporter A1; ERS, endoplasmic reticulum stress; VC, vascular calcification; G6PD, glucose-6-phosphate dehydrogenase; KLF5, Krüppel-like factor 5; Cx43, connexin 43; HO-1, heme oxygenase-1; MEF2C, myosin enhancer factor-2c; Akt, protein kinase B; eNOS, endothelial nitric oxide synthase; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1 alpha; I/R, ischemia/reperfusion; CSE, cystathionine gamma-lyase; PTP, mitochondrial permeability transition pore.