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. 2021 Mar 6;28(5):454–466. doi: 10.5551/jat.RV17048

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