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Rev Physiol Biochem Pharmacol. 2018;174:81-156. doi: 10.1007/112_2017_7.

Gaseous Signaling Molecules in Cardiovascular Function: From Mechanisms to Clinical Translation.

Author information

1
Department of Convergence Biomedical Science, Cardiovascular and Metabolic Disease Center, College of Medicine, Inje University, Busan, Republic of Korea.
2
Laboratory of Ion Channel Research, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
3
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, Department of Health Sciences and Technology, BK21 Plus Project Team, Cardiovascular and Metabolic Disease Center, Inje University, Busan, Republic of Korea. phyhanj@inje.ac.kr.

Abstract

Carbon monoxide (CO), hydrogen sulfide (H2S), and nitric oxide (NO) constitute endogenous gaseous molecules produced by specific enzymes. These gases are chemically simple, but exert multiple effects and act through shared molecular targets to control both physiology and pathophysiology in the cardiovascular system (CVS). The gases act via direct and/or indirect interactions with each other in proteins such as heme-containing enzymes, the mitochondrial respiratory complex, and ion channels, among others. Studies of the major impacts of CO, H2S, and NO on the CVS have revealed their involvement in controlling blood pressure and in reducing cardiac reperfusion injuries, although their functional roles are not limited to these conditions. In this review, the basic aspects of CO, H2S, and NO, including their production and effects on enzymes, mitochondrial respiration and biogenesis, and ion channels are briefly addressed to provide insight into their biology with respect to the CVS. Finally, potential therapeutic applications of CO, H2S, and NO with the CVS are addressed, based on the use of exogenous donors and different types of delivery systems.

KEYWORDS:

Carbon monoxide; Cardiovascular; Hydrogen sulfide; Ion channel; Mitochondria; Nitric oxide; Translational medicine

PMID:
29372329
DOI:
10.1007/112_2017_7
[Indexed for MEDLINE]

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