The pathogenesis of cardiovascular disease (CVD) is complex and multifactorial, and inflammation plays a central role. Inflammasomes are multimeric protein complexes that are activated in a 2-step manner in response to infection or tissue damage. Upon activation the proinflammatory cytokines, interleukins-1β and -18 are released. In the last decade, the evidence that inflammasome activation plays an important role in CVD development became stronger. We discuss the role of different inflammasomes in the pathogenesis of CVD, focusing on atherosclerosis and heart failure. This review also provides an overview of existing experimental studies and clinical trials on inflammasome inhibition as a therapeutic target in these disorders.
Keywords: ACS, acute coronary syndrome; AIM2, absent in melanoma 2; ASC, apoptosis associated speck-like protein; ATP, adenosine triphosphate; CAD, coronary artery disease; CRP, C-reactive protein; CVD, cardiovascular disease; DAMP, damage associated molecular pattern; GSDMD, gasdermin-D; GSDMD-NT, gasdermin-D N-terminal; HF, heart failure; HFpEF, HF with preserved ejection fraction; HFrEF, HF with reduced ejection fraction; IL, interleukin; IL-1; LDL, low-density lipoprotein; LV, left ventricular; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NF-κB, nuclear factor κB; NLR, NOD-like receptor; NLRP3; NLRP3, NOD-like receptor family pyrin domain containing 3; NOD, nucleotide-binding oligomerization domain; PRR, pattern recognition receptor; STEMI, ST-elevation myocardial infarction; TLR, toll-like receptor; atherosclerosis; cardiovascular disease; heart failure; inflammasome.
© 2022 The Authors.