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.
