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越来越多的证据支持H2S是第三种内源性气体信号分子。内源性H2S以半胱氨酸为底物在胱硫醚-β-合成酶或胱硫醚-γ-裂解酶催化下生成。在心血管系统中,H2S作用于血管平滑肌KATP通道和Cl-/HCO3-交换体舒张血管,并参与血压中枢调节。此外,H2S促进血管平滑肌的凋亡并抑制其增殖。H2S也作用于心肌KATP通道调节心肌收缩。病理状态下,H2S参与多种心血管疾病的发生,如高血压、心肌缺血/再灌注损伤,外源性的H2S可减轻疾病程度。
There is growing evidence that H2S is the third endogenous gas signaling molecule. Endogenous H2S is generated on the basis of cysteine catalyzed by cystathionine-β-synthase or cystathionine-γ-lyase. In the cardiovascular system, H2S acts on vasodilator KATP channels and Cl- / HCO3- exchangers to relax blood vessels and is involved in the regulation of blood pressure centers. In addition, H2S promotes vascular smooth muscle apoptosis and inhibits its proliferation. H2S also acts on myocardial KATP channels to regulate myocardial contractility. Under pathological conditions, H2S is involved in a variety of cardiovascular diseases, such as hypertension, myocardial ischemia / reperfusion injury, exogenous H2S can reduce the degree of disease.