Figure 5. Oxidative stress and the inflammasome in hypertension.

Prohypertensive factors induce activation of NLRP3 inflammasome through ROS. ROS influences signal 1 (cytokines, pathogen-associated molecular patterns (PAMPS), danger-associated molecular patterns (DAMPS)), leading to activation of NFkB and gene expression of components of the inflammasome. ROS also influence signal 2, by PAMPS, DAMPS, oxidized LDL (oxLDL), oxidized phospholipids (oxPL), ATP, Ang II, ET-1, aldosterone (aldo) and cations (K⁺, Ca²⁺, Na⁺). These processes lead to assembly of the inflammasome complex (NLRP3, ASC and pro-caspase 1), and consequent activation of caspase 1, cleavage of pro-IL-1β and pro-IL-18, and production of active forms of IL-1β and IL-18, which increase the inflammatory response, fibrosis and vascular remodelling in hypertension. MR, mineralocorticoid receptor; ASC - Apoptosis-Associated Speck-Like Protein Containing CARD; question mark (?) indicates possible effect.