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NLRP3 Inflammasome in Acute Myocardial Infarction

Mauro, Adolfo G. PhD*,†; Bonaventura, Aldo MD*,‡; Mezzaroma, Eleonora PhD*,†,§; Quader, Mohammed MD*,¶,║; Toldo, Stefano PhD*,†,¶

Journal of Cardiovascular Pharmacology: September 2019 - Volume 74 - Issue 3 - p 175–187
doi: 10.1097/FJC.0000000000000717
Invited Review Article
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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.

*VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA;

Johnson Center for Critical Care Medicine Pulmonary Research, Virginia Commonwealth University, Richmond, VA;

Department of Internal Medicine, First Clinic of Internal Medicine, University of Genoa, Genoa, Italy;

§Pharmacotherapy and Outcomes Sciences, Virginia Commonwealth University, Richmond, VA;

Department of Cardiothoracic Surgery, Virginia Commonwealth University, Richmond, VA; and

Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, VA.

Reprints: Stefano Toldo, PhD, VCU Pauley Heart Center, Virginia Commonwealth University, Box 980281, Richmond, VA 23298 (e-mail: Stefano.toldo@vcuhealth.org).

S. Toldo has received research support from Olatec. A. G. Mauro is supported by an American Heart Association pre-doctoral grant. M. Quader is supported by a Scientist Development Grant from the American Heart Association and from a Merit Review Award from the Veterans Health Administration.

The authors report no conflicts of interest.

Received March 08, 2019

Accepted June 10, 2019

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