FIG. 1.

The mechanism of NLRP3 inflammasome activation and proposed association with hypertension. TLR recognizes PAMPs and DAMPs, and leads to the translocation of NF-κB to the nucleus, which increases the expression of pro-IL-1β, pro-IL-18, and components of NLRP3 inflammasome complex. The activated NLRP3 inflammasome activates caspase 1, and leads to the cleavage of pro-IL-1β and pro-IL-18 into cytokines IL-1β and IL-18, which are released into the extracellular space and ultimately bloodstream, inducing inflammatory response. Existing evidence suggests that this NLRP3-induced inflammatory response may contribute to hypertension and SSBP. NADPH oxidase-induced ROS generation, which is increased in hypertension, also potentially mediates NLRP3 inflammasome activation and assembly. DAMPs, damage-associated molecular patterns; IL, interleukin; NADPH, nicotinamide adenine dinucleotide phosphate; NF-κB, nuclear factor-kappaB; NLRP3, NOD-like receptor family pyrin domain containing 3; PAMPs, pathogen-associated molecular patterns; ROS, reactive oxygen species; SSBP, salt sensitivity of blood pressure; TLR, Toll-like receptor. Color images are available online.