NLRP3: A Novel Mediator in Cardiovascular Disease

Table 1

Possible therapeutic approaches targeting the NLRP3 inflammasome.

Experiment types	Model	Treatment	Effects	Ref.
Animal experiments or in vitro experiments	Apoe^−/− mouse model, high-fat diet	Arglabin	Reduced the secretion of IL-1β and IL-18, convert proinflammatory M1 macrophage into anti-inflammatory M2 macrophage, induce autophagy, decrease cholesterol level in plasma, reduce atherosclerosis size	[51]
	Type 2 diabetic rat model	Rosuvastatin	Inhibited the NLRP3 inflammasome and suppressed the MAPK pathway	[53]
	AMI mouse model	16673-34-0	Reduced the NLRP3 inflammasome activation in cardiomyocytes, decreased the infarct size	[57]
	AMI mouse model	Colchicine	Inhibited the mRNA expression level of NLRP3 inflammasome components, improved the survival rate	[58]
	In vitro hypoxia model	Pigment epithelium-derived factor (PEDF)	Inhibited the NLRP3 inflammasome by eliminating mitochondrial damage and thus mtROS accumulation	[56]
Clinical trials	Patients with coronary artery disease	Atorvastatin or rosuvastatin for 8 months	Reduced the expression level of the NLRP3 inflammasome and slowed the progression of atherosclerosis in the atorvastatin, but not the rosuvastatin, group	[52]
	Patients with ST-elevation MI	Colchicine	Reduced the infarct size	[59]
	Patients with coronary disease	Colchicine	Decreased the incidence of cardiovascular events	[60]