Sterile inflammation and the NLRP3 inflammasome in cardiometabolic disease

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Inflammation plays an important role in the pathophysiology of cardiometabolic diseases. Sterile inflammation, a non-infectious and damage-associated molecular pattern (DAMP)-induced innate response, is now well-established to be closely associated with development and progression of cardiometabolic diseases. The NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome is well-established as a major player in sterile inflammatory responses. It is a multimeric cytosolic protein complex which regulates the activation of caspase-1 and subsequently promotes cleavage and release of interleukin (IL)-1 family cytokines, which have a deleterious impact on the development of cardiometabolic diseases. Therefore, targeting NLRP3 itself or the downstream consequences of NLRP3 activation represent excellent potential therapeutic targets in inflammatory cardiometabolic diseases. Here, we review our current understanding of the role which NLRP3 inflammasome regulation plays in cardiometabolic diseases such as obesity, diabetes, non-alcoholic steatohepatitis (NASH), atherosclerosis, ischemic heart disease and cardiomyopathy. Finally, we highlight the potential of targeting NLPR3 or related signaling molecules as a therapeutic approach.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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