Table 1.

Cardiac phenotype and function in mice with AT2 overexpression (TG) or knock out (KO).

Mouse model		Strain	Baseline	Disease state	References
			↔HW/BW	AS: ↔ HW/BW
AT2 TG mice (cardiomyocyte-specific, α-MHC)		C57BL/6	↑PW	Ang II: ↔ HW/BW, ↓HR	[15, 18, 19]
			↑EF%	MI: ↔LVMI, ↑PW, ↑EF%
			↑LVW/BW,
			↓wall thickness
			↑interstitial collagen
	AT2highTG		↑myocyte area and length		[14]
AT2 TG mice (ventricular myocyte-specific, MLC-2v)			↓LV contractile function
		FVB/n	↑apoptosis
				AS: ↔LVW/BW
				↔wall thickness
				↓myocyte diameter
	AT2lowTG		↔ cardiac morphology and function	↓interstitial collagen	[21]
				↓LVSP
				↓LVEDP
			↑BP	AS: No hypertrophy
			↑HR	↓interstitial collagen
			↓LVW/BW	↔cardiac function
AT2 KO mice		C57BL/6	↓wall thickness	Ang II: No hypertrophy	[16, 22, 23]
			↓LVMI	↔BP
			↔contractile function	↓interstitial collagen
				↑diastolic function
			↔BP	AS: ↔hypertrophy
			↔ cardiac morphology	↑perivascular fibrosis
AT2 KO mice		FVB/n		↑coronary arterial thickening
				AMI: ↑LVW/BW	[17, 24, 25]
				↑Lung/BW
				↓EF%

HW: heart weight; LVW: left ventricular weight; BP: blood pressure; HR: heart rate; LVMI: left ventricular mass index; PW: posterior wall thickness; EF: ejection fraction; AS: aortic stenosis; Ang II: Ang II infusion; MI: myocardial infarction.