Abstract
The NLRP3 inflammasome is an intracellular, multimeric protein complex that initiates a potent inflammatory response to danger signals. After acute myocardial infarction, NLRP3 inflammasome-dependent inflammation promotes adverse left ventricular remodeling and recurrent atherosclerotic events. Selective and nonselective inhibitors of the NLRP3 inflammasome or its downstream effectors (interleukin-1β and interleukin-18) may prevent adverse left ventricular remodeling and recurrent atherosclerotic events. In this review, we highlight strategies to inhibit NLRP3 inflammasome activity and their potential roles in the management of acute myocardial infarction.
MeSH terms
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Animals
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Anti-Inflammatory Agents / adverse effects
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Anti-Inflammatory Agents / pharmacokinetics
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Anti-Inflammatory Agents / therapeutic use*
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Cardiovascular Agents / adverse effects
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Cardiovascular Agents / pharmacokinetics
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Cardiovascular Agents / therapeutic use*
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Humans
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Inflammasomes / antagonists & inhibitors*
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Inflammasomes / immunology
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Inflammasomes / metabolism
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Inflammation / drug therapy*
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Inflammation / immunology
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Inflammation / metabolism
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Inflammation / pathology
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Inflammation Mediators / antagonists & inhibitors*
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Inflammation Mediators / immunology
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Inflammation Mediators / metabolism
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Molecular Targeted Therapy
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Myocardial Infarction / drug therapy*
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Myocardial Infarction / immunology
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Myocardial Infarction / metabolism
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Myocardial Infarction / pathology
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NLR Family, Pyrin Domain-Containing 3 Protein / antagonists & inhibitors*
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NLR Family, Pyrin Domain-Containing 3 Protein / immunology
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NLR Family, Pyrin Domain-Containing 3 Protein / metabolism
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Signal Transduction
Substances
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Anti-Inflammatory Agents
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Cardiovascular Agents
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Inflammasomes
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Inflammation Mediators
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NLR Family, Pyrin Domain-Containing 3 Protein