AKT1 and heart failure: XYT has been shown to reduce heart failure in animal models[18,25–30] by lowering serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), endothelin-1 (ET-1), angiotensin II (Ang II), aldosterone (ALD), improving cardiac ultrastructure, intervention of (Akt/AMPK)-mTOR signaling pathway, down-regulation of autophagy, reducing myocardial apoptosis, increasing left ventricular ejection fraction and shortening rate, delaying ventricular remodeling, inhibiting myocardial fibrosis, and improving cardiac function.