Table 1.

Examples of commonly used mouse models of abdominal aortic aneurysm (AAA). Key histological and pathological features of each model and their rupture characteristics when compared to human AAA are outlined.

Model	Key Features	Rupture Characteristics	Reference
Genetic
Timp-1 -/- Deficient in TIMP-1 gene	Proteolysis ECM degradation Inflammation Aneurysms in both the thoracic and abdominal regions of the aorta	No ruptures reported	[34,35,36,37,38,39]
ApoE -/- Deficient in ApoE gene	Dyslipidemia Atherosclerosis Require other AAA induction agents such as high fat diet or chemical induction	No ruptures reported in genetic deficiency alone	[40,41,42,43,44,45]
Blotchy and Lox -/-	Lack crosslinks between elastin and collagen fibers Elastin fragmentation VSMC apoptosis Aneurysms along the full length of the aorta	No ruptures reported in most studies One study reports that males do rupture and females do after hydrocortisone treatment	[46,47,48,49] [31]
Overexpression of Renin and Angiotensinogen	Hypertension, Inflammation Medial degeneration Require high salt intake Aneurysms and ruptures Aneurysms in the thoracic and abdominal regions of the aorta	No ruptures reported	[50,51]
Chemical
CaCl2 Painting solubilised CaCl2 on the exposed IRA	Aortic calcification Medial degeneration Inflammatory cells infiltration	No ruptures reported	[32,52,53,54]
CaPO4 Painting solubilised CaPO4 on the exposed IRA	Aortic calcification Medial degeneration Inflammatory cells infiltration	No ruptures reported	[55,56]
AngII infusion Delivering AngII through subcutaneously implanted osmotic pumps	Acute aortic dissections, aneurysms and ruptures Upregulation of chemokines and pro-inflammatory cytokines Leukocyte infiltration ECM degeneration VSMC apoptosis	Ruptures often occur within first week of AngII infusion in the arch, thoracic and SRA regions	[33,57,58,59,60]
AngII + BAPN AngII infusion to mice that had received BAPN	Leads to higher incidence of AAA Medial ECM degeneration VSMC apoptosis Dissections are common with presence of ILT and IMT	Fatal medial ruptures in the IRA	[61,62,63,64]
AngII + Leptin Peri-aortic application of Leptin in the ApoE-/- mouse combined with AngII infusion	ECM degeneration MMP up-regulation Macrophage infiltration Dissections and IMT are present	No ruptures reported	[65]
AngII + anti-TGF-β antibody	Aortic dissection Enhanced monocyte infiltration Increased MMP-12 activity	Increased rupture in both the ascending aorta and SRA	[66,67]
Elastase perfusion Elastase is delivered through a catheter placed in the IRA	Inflammation Medial degeneration and ILT present	No ruptures reported	[68,69,70,71]
Elastase + TGF-β activity Blocking Combined adventitial application of Elastase and neutralizing TGF-β activity by mouse monoclonal antibody	Enhanced elastin degradation Ongoing inflammation Presence of large amount of ILT	Fatal rupture in IRA	[72,73]
Elastase + BAPN Combined adventitial application of Elastase on mice that had received BAPN	Higher AAA incidence Medial ECM degeneration VSMC apoptosis ILT presence	Fatal rupture in IRA	[62,74]

Abbreviations: AngII, angiotensin II; ApoE, apolipoprotein E; BAPN, β-aminopropionitrile monofumarate; CaCl₂, calcium chloride, CaPO₄, calcium phosphate; ECM, extracellular matrix; ILT, intra-luminal thrombus; IMT, intra-mural thrombus; IRA, infrarenal aorta; Lox, lysyl oxidase; MMP, matrix metalloproteinase; SRA, suprarenal aorta; TIMP, tissue inhibitor of metalloproteinase; VSMC, vascular smooth muscle cells.