NLRP3 inflammasome as a treatment target in atherosclerosis: A focus on statin therapy

Activation of NOD-like receptor (NLR) family and pyrin domain containing 3 (NLRP3) inflammasome contributes to inflammation and may lead to atherosclerosis. The NLRP3 inflammasome as a molecular platform regulates the activation of ATP signaling, K+ efflux, cathepsin-B activity, lysosomal function and pro-inflammatory cytokines (i.e. IL-1β and IL-18). Statins has been widely prescribed for the treatment of hyperlipidemia and cardiovascular diseases. In addition to lipid-lowering effect, statins have immunomodulatory, anti-inflammatory, antioxidant and antiapoptotic functions. An increasing number of studies indicated NLRP3 inflammasome and their downstream mediators as important targets for statin drugs in inflammatory diseases. In this review, we discussed different aspect of the NLRP3 inflammasome signaling pathways and focused on the effect of statin drugs on NLRP3 inflammasomes in association to atherosclerosis in order to elucidate possible targets for future research and clinical settings. •Activation of NLRP3 inflammasome contributes to inflammation and may lead to atherosclerosis.•Statins has been widely prescribed for the treatment of hyperlipidemia and cardiovascular diseases.•In addition to lipid-lowering effect, statins have anti-inflammatory functions.•NLRP3 inflammasome and their downstream mediators as important targets for statins•We review the effect of statins on NLRP3 inflammasome.