NLRP3 Inflammasome in Acute Myocardial Infarction

Adolfo G Mauro; Aldo Bonaventura; Eleonora Mezzaroma; Mohammed Quader; Stefano Toldo

doi:10.1097/FJC.0000000000000717

NLRP3 Inflammasome in Acute Myocardial Infarction

J Cardiovasc Pharmacol. 2019 Sep;74(3):175-187. doi: 10.1097/FJC.0000000000000717.

Authors

Adolfo G Mauro^{1

2}, Aldo Bonaventura^{1

3}, Eleonora Mezzaroma^{1

2

4}, Mohammed Quader^{1

5

6}, Stefano Toldo^{1

2

5}

Affiliations

¹ VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA.
² Johnson Center for Critical Care Medicine Pulmonary Research, Virginia Commonwealth University, Richmond, VA.
³ Department of Internal Medicine, First Clinic of Internal Medicine, University of Genoa, Genoa, Italy.
⁴ Pharmacotherapy and Outcomes Sciences, Virginia Commonwealth University, Richmond, VA.
⁵ Department of Cardiothoracic Surgery, Virginia Commonwealth University, Richmond, VA.
⁶ Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, VA.

PMID: 31356555
DOI: 10.1097/FJC.0000000000000717

Abstract

Acute myocardial infarction (AMI) is associated with the induction of a sterile inflammatory response that leads to further injury. The NACHT, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome is a macromolecular structure responsible for the inflammatory response to injury or infection. NLRP3 can sense intracellular danger signals, such as ischemia and extracellular or intracellular alarmins during tissue injury. The NLRP3 inflammasome is primed and triggered by locally released damage-associated molecular patterns and amplifies the inflammatory response and cell death through caspase-1 activation. Here, we examine the scientific evidence supporting a role for NLRP3 in AMI and the available strategies to inhibit the effects of the inflammasome. Our focus is on the beneficial effects seen in experimental models of AMI in preclinical animal models and the initial results of clinical trials.

Publication types

Review

MeSH terms

Animals
Anti-Inflammatory Agents / therapeutic use
Cardiovascular Agents / therapeutic use
Cytokines / metabolism
Humans
Inflammasomes / antagonists & inhibitors
Inflammasomes / immunology
Inflammasomes / metabolism*
Inflammation / drug therapy
Inflammation / immunology
Inflammation / metabolism*
Inflammation / pathology
Inflammation Mediators / antagonists & inhibitors
Inflammation Mediators / immunology
Inflammation Mediators / metabolism*
Myocardial Infarction / drug therapy
Myocardial Infarction / immunology
Myocardial Infarction / metabolism*
Myocardial Infarction / pathology
Myocardium / immunology
Myocardium / metabolism*
Myocardium / pathology
NLR Family, Pyrin Domain-Containing 3 Protein / antagonists & inhibitors
NLR Family, Pyrin Domain-Containing 3 Protein / immunology
NLR Family, Pyrin Domain-Containing 3 Protein / metabolism*
Pyroptosis
Signal Transduction

Substances

Anti-Inflammatory Agents
Cardiovascular Agents
Cytokines
Inflammasomes
Inflammation Mediators
NLR Family, Pyrin Domain-Containing 3 Protein