Emergence of hydrogen sulfide as an endogenous gaseous signaling molecule in cardiovascular disease.
Emergence of hydrogen sulfide as an endogenous gaseous signaling molecule in cardiovascular disease.
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DOI:
10.1161/circresaha.114.300505
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发表时间:
2014-02-14
影响因子:
20.1
通讯作者:
Lefer DJ
中科院分区:
文献类型:
--
作者:
Polhemus DJ;Lefer DJ
Long recognized as a malodorous and highly toxic gas, recent experimental studies have revealed that hydrogen sulfide (H2S) is produced enzymatically in all mammalian species including man and exerts a number of critical actions to promote cardiovascular homeostasis and health. During the past 15 years, scientists have determined that H2S is produced by three endogenous enzymes and exerts powerful effects on endothelial cells, smooth muscle cells, inflammatory cells, mitochondria, endoplasmic reticulum, and nuclear transcription factors. These effects have been reported in multiple organ systems and the vast majority of data clearly indicate that H2S produced by the endogenous enzymes exerts cytoprotective actions. Recent preclinical studies investigating cardiovascular diseases have demonstrated that the administration of physiological or pharmacological levels of H2S attenuates myocardial injury, protects blood vessels, limits inflammation, and regulates blood pressure. H2S has emerged as a critical cardiovascular signaling molecule similar to nitric oxide (NO) and carbon monoxide (CO) with a profound impact on the heart and circulation (Figure 1). Our improved understanding of how H2S elicits protective actions, coupled with the very rapid development of novel H2S releasing agents, has resulted in heightened enthusiasm for the clinical translation of this ephemeral gaseous molecule. This review will examine our current state of knowledge regarding the actions of H2S within the cardiovascular system with an emphasis on the therapeutic potential and molecular crosstalk between H2S, NO, and CO.