Journal of Inflammation Research (Dec 2021)
Spotlight on NLRP3 Inflammasome: Role in Pathogenesis and Therapies of Atherosclerosis
Abstract
Chunteng Jiang,1,2 Santuan Xie,1 Guang Yang,3 Ningning Wang3 1Department of Internal Medicine, The Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning, People’s Republic of China; 2Department of Cardiology and Pneumology, University Medical Center of Göttingen, Georg-August-University of Göttingen, Göttingen, Lower Saxony, Germany; 3Department of Food Nutrition and Safety, School of Public Health, Dalian Medical University, Dalian, Liaoning, People’s Republic of ChinaCorrespondence: Guang Yang; Ningning Wang Email [email protected]; [email protected]: Inflammation is an intricate biological response of body tissues to detrimental stimuli. Cardiovascular disease (CVD) is the leading cause of death worldwide, and inflammation is well documented to play a role in the development of CVD, especially atherosclerosis (AS). Emerging evidence suggests that activation of the NOD-like receptor (NLR) family and the pyridine-containing domain 3 (NLRP3) inflammasome is instrumental in inflammation and may result in AS. The NLRP3 inflammasome acts as a molecular platform that triggers the activation of caspase-1 and the cleavage of pro-interleukin (IL)-1β, pro-IL-18, and gasdermin D (GSDMD). The cleaved GSDMD forms pores in the cell membrane and initiates pyroptosis, inducing cell death and the discharge of intracellular pro-inflammatory factors. Hence, the NLRP3 inflammasome is a promising target for anti-inflammatory therapy against AS. In this review, we systematically summarized the current understanding of the activation mechanism of NLRP3 inflammasome, and the pathological changes in AS involving NLRP3. We also discussed potential therapeutic strategies targeting NLRP3 inflammasome to combat AS.Keywords: cardiovascular disease, atherosclerosis, NLRP3 inflammasome, mechanisms, therapeutic strategies
