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. Author manuscript; available in PMC: 2022 Apr 2.
Published in final edited form as: Circ Res. 2021 Apr 1;128(7):908–933. doi: 10.1161/CIRCRESAHA.121.318052

Figure 2: The NLRP3 Inflammasome in Hypertension.

Figure 2:

The NLRP3 inflammasome begins its activation through a priming step mediated by the transcription factor NF-κB, which upregulates inflammasome components NLRP3 and pro-IL-1β. Multiple endogenous vasoactive molecules including Endothelin-1, Aldosterone, Angiotensin II, and NaCl can serve as priming stimuli. A second activation step is needed to trigger the formation of the components into the NLRP3 inflammasome signaling complex. Once assembled, caspase-1 proteolytically cleaves pro-IL-1β into the released IL-1β. NLRP3 inflammasome activation has been shown to play a role in the induction of renal injury and vascular remodeling, ultimately leading to hypertension. (Illustration Credit: Ben Smith)