Mechanism of NLRP3 Activation, Associated Cardiovascular Complications and Update on its Inhibitors Acting as Cardioprotective Agents

Cardiovascular disorders (CVDs) are a major healthcare issue worldwide and are accountable for significant mortality and morbidity. Despite advancements in cellular, molecular, physiological and pathological understanding, a comprehensive understanding of CVDs is still lacking. Hence, a better understanding of pathological changes is needed to develop a potential cardioprotective agent. In recent times, NLRP3 inflammasome has been extensively studied in various disease conditions, including CVDs. The activation of NLRP3 inflammasome has been found to be positively correlated with various CVDs, such as hypertension, angina, arrhythmia, cardiac fibrosis, myocardial infarction, heart failure, etc. Moreover, a number of NLRP3 inflammasome activators have been explored for their role in CVDs, and the outcomes of these studies are found to be promising. Therefore, in the present manuscript, we have discussed the structural component of NLRP3 inflammasome, its molecular mechanism of activation, and the outcome of various NLRP3 inflammasome inhibitors in CVDs. We found that NLRP3 inflammasome is an indispensable player of pathogenesis in CVDs, and thus, targeting this inflammasome can be an effective approach for managing and treating these diseases.

Keywords: Myocardial infarction and MCC950, NLRP3 Inflammasome, Nuclear factor kappa B (NF-kB), Oxidative stress.