NLRP3 inflammasome: A key player in cardiac fibroblast to myofibroblast transition

Cardiac fibrosis is one of the main causes of mortality from cardiovascular disorders and may result in heart failure, irregular heartbeats, and sudden cardiac death. Multiple complex mechanisms involved in cardiac fibrosis are beyond the scope of current treatments. Inflammasomes are significant inflammatory modulators. Inflammasome impairment may exacerbate heart failure. The most specific inflammasome associated with inflammatory and cardiovascular disorders is Nucleotide-binding oligomerisation domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3). Pathogen-associated molecular patterns and damage-associated patterns are recognised by the intracellular sensor NLRP3, which causes the NLRP3 inflammasome to assemble and become active. Thus, a greater awareness of the pathological function of the inflammasome in heart fibrosis may lead to new approaches to the disease's early detection and management. Understanding the inflammasome's regulatory functions in fibrosis of the heart in its entire form has been made possible by recent research on the subject. The most recent studies on the roles of the NLRP3 inflammasome in different cardiac conditions are included in this review. According to recent research, the NLRP3 inflammasome promotes a number of inflammatory reactions and is linked to myofibroblast development, mitochondrial modulation, and pyroptosis in cardiac fibrosis. These discoveries provide light on the critical function of the NLRP3 inflammasome in the aetiology of heart fibrosis, which may help establish novel paths for therapy and prevention.