Abstract
The cardiac Na+-Ca2+ exchanger (NCX) plays an essential role in regulating Ca2+ under physiological and pathophysiological conditions. In its forward mode of operation, which predominates under physiological conditions, it extrudes the Ca2+ that enters the cardiac myocyte on a beat-to-beat basis. During ischemia and reperfusion, increased intracellular Na+ leads to a decrease in Ca2+ efflux and enhanced Ca2+ influx via the NCX, potentially leading to Ca2+ overload, which is one of the major pathophysiological mechanisms for ischemia-reperfusion injury. Novel NCX inhibitors discovered in recent years have shown great promise in attenuating ischemia-reperfusion injury.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Aniline Compounds / pharmacology
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Animals
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Anti-Arrhythmia Agents / pharmacology
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Cardiotonic Agents / pharmacology
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Guanidines / pharmacology
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Humans
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Myocardial Reperfusion Injury / physiopathology
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Myocardial Reperfusion Injury / prevention & control*
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Phenyl Ethers / pharmacology
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Sodium-Calcium Exchanger / antagonists & inhibitors*
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Sodium-Calcium Exchanger / physiology
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Sodium-Hydrogen Exchangers / antagonists & inhibitors
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Sulfones / pharmacology
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Thiourea / analogs & derivatives*
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Thiourea / pharmacology
Substances
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2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonate
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Aniline Compounds
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Anti-Arrhythmia Agents
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Cardiotonic Agents
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Guanidines
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Phenyl Ethers
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SEA 0400
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Sodium-Calcium Exchanger
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Sodium-Hydrogen Exchangers
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Sulfones
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cariporide
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Thiourea