ISSN: 2155-9880
+44 1300 500008
Jasna Ajdukovic
The inflammasome is a cytosolic protein complex involved in the pathogenesis of atherosclerosis. The NLRP3 inflammasome can be activated by a wide range of stimuli, including intracellular cholesterol crystals The NLRP3 inflammasome is up-regulated within the myocardium after myocardial infarction (MI), primarily in noncardiomyocytes (i.e. fibroblasts). Its deficiency markedly improves myocardial function and reduces infarct size after ex vivo myocardial ischaemia-reperfusion injury I/R. NLRP3 inflammasome is up-regulated in myocardial fibroblasts after MI, potentially contributing to infarct size after myocardial I/R. NLRP3 inhibitors and mechanism of action, Glyburide, Apigenin, Parthenolide, Cysteinyl leukotriene receptor antagonist, Inhibitors of P2X7, Scropolioside B, Cyclooxygenase-2 (COX-2) inhibitors, Intravenous immunoglobulin, Resveratrol, C3a Pt and inhibitors of C3a receptor, Atorvastatin, Zinc, Umbelliferone (UMB), omega-3 fatty acids, Ethanol. Modulation of the inflammasome may represent a unique therapeutic strategy to limit cell death and prevent heart failure after AMI. Inflammasome inhibitors may improve current treatment approach.