Modulatory Mechanism of NLRP3 Inflammasome in Heart Diseases: “An Enigma Wrapped in a Riddle”

Despite breakthroughs in therapy over the prior two decades, heart failure is considered the foremost cause of mortality globally. The inflammasome plays a pivotal role in the advancement of heart failure, abdominal aortic aneurysm, atherosclerosis, diabetic cardiomyopathy, hypertension, dilated cardiomyopathy, cardiac remodeling and calcific aortic valve disease. The NLRP3 inflammasome is a crucial multi-protein signaling platform that tightly regulates inflammatory responses. It regulates antimicrobial host defense, which causes pyroptosis through caspase-1 activation by the eventual production of pro-inflammatory cytokines. The investigation of the NLRP3 inflammasome in various cardiovascular diseases may reveal critical disease triggers and endogenous modulators, leading to the development of new therapeutic interventions in the future. The target of this chapter is to summarise the recent literature describing the activation mechanism of the NLRP3 inflammasome by implicating different inflammatory pathways in the pathophysiology of heart failure.

Keywords: Caspase-1, Heart failure, IL-1β, Inflammation, NLRP3 inflammasome.