NLRP3 Inflammasome in Acute Myocardial Infarction

被引:100
作者
Mauro, Adolfo G. [1 ,2 ]
Bonaventura, Aldo [1 ,3 ]
Mezzaroma, Eleonora [1 ,2 ,4 ]
Quader, Mohammed [1 ,5 ,6 ]
Toldo, Stefano [1 ,2 ,5 ]
机构
[1] Virginia Commonwealth Univ, VCU Pauley Heart Ctr, Box 980281, Richmond, VA 23298 USA
[2] Virginia Commonwealth Univ, Johnson Ctr Crit Care Med Pulm Res, Richmond, VA USA
[3] Univ Genoa, Dept Internal Med, Clin Internal Med 1, Genoa, Italy
[4] Virginia Commonwealth Univ, Pharmacotherapy & Outcomes Sci, Richmond, VA USA
[5] Virginia Commonwealth Univ, Dept Cardiothorac Surg, Richmond, VA USA
[6] Hunter Holmes McGuire Vet Affairs Med Ctr, Richmond, VA USA
关键词
NLRP3; inflammasome; acute myocardial infarction; interleukin-1; beta; interleukin-18; caspase-1; ISCHEMIA-REPERFUSION INJURY; PRESERVES CARDIAC-FUNCTION; IL-1 RECEPTOR ANTAGONIST; FACTOR-KAPPA-B; INTERLEUKIN-1; BLOCKADE; HEART-FAILURE; CELL-DEATH; BLOCKING INTERLEUKIN-1; PRESSURE-OVERLOAD; ACTIVATION;
D O I
10.1097/FJC.0000000000000717
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:175 / 187
页数:13
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