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.