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This activation attenuates angiotensin II (Ang II)driven cardiac remodelingevidenced by downregulated expression of hypertrophic markers (ANP, BNP, and -MHC), improved systolic function in transverse aortic constriction (TAC) mice (increased ejection fraction [EF%] and fractional shortening [FS%], alongside reduced left ventricular internal diameter [LVID] and heart weight-to-body weight ratio [HW/BW]), and suppression of fibrotic progression (decreased expression of Col1a1, Col3a1, fibronectin, and -smooth muscle actin [-SMA])
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due in part to genetic variation [8]
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