Review Article

Genetically Modified Mouse Models Used for Studying the Role of the AT2 Receptor in Cardiac Hypertrophy and Heart Failure

Table 1

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

Mouse modelStrainBaselineDisease stateReferences

HW/BWAS: HW/BW
AT2 TG mice (cardiomyocyte-specific, α-MHC)C57BL/6↑PWAng II: HW/BW, HR[15, 18, 19]
↑EF%MI: LVMI, ↑PW, ↑EF%

↑LVW/BW,
wall thickness
↑interstitial collagen
TG↑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
TG cardiac morphology and function    interstitial collagen[21]
    LVSP
    LVEDP

↑BPAS: No hypertrophy
↑HR    interstitial collagen
LVW/BW    cardiac function
AT2 KO miceC57BL/6wall thicknessAng II: No hypertrophy[16, 22, 23]
LVMI   BP
contractile function   interstitial collagen
   ↑diastolic function

BPAS: hypertrophy
cardiac morphology    ↑perivascular fibrosis
AT2 KO miceFVB/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.