Table 2. Effect of genetic deficiency of individual NLRP3 inflammasome components on experimental AAAs.

Mouse strain	AAA model	Gene knockout	Influence on experimental AAAs	References
ApoE －/－	Ang II infusion	NLRP3 －/－ , ASC －/－ , or caspase-1－/－	•Reduce AAA severity, aortic inflammatory cell infiltration and the serum levels of IL-1β, MMP2, MMP9	[74] Usui F et al. Arterioscler Thromb Vasc Biol 35: 127-136, 2015.
ApoE －/－	Ang II infusion and homocysteine diet	Lentivirus-mediated NLRP3 silencing	•Reduced aneurysmal aortic diameter and severity •Downregulated the expression levels of aortic inducible nitric oxide synthase and myofibroblast markers •Reduced aortic MMP9 activity	[78] Sun W et al. J Mole Cell Cardiol 81: 96-106, 2015.
C57BL/6	Lactobacillus casei cell-wall extract injection	Caspase-1 －/－ or NLRP3 －/－	•Prevented AAA formation	[77] Wakita D et al. Arterioscler Thromb Vasc Biol 36: 886-897, 2016.
C57BL/6	Ang II infusion and high fat diet	Caspase-1 －/－ or NLRP3 －/－	•Reduced aneurysm incidence and maximal diameter •Degraded aortic contractile proteins	[87] Wu D et al. Arterioscler Thromb Vasc Biol 37: 694-706, 2017.

AAA: Abdominal aortic aneurysm. Ang II: Angiotensin II. ApoE: Apolipoprotein E. ASC: Apoptosis-associated speck-like protein containing a caspase recruitment domain. IL: Interleukin. MMP: Matrix metalloproteinase. -/-: Deficient mice