The pathogenesis of HFpEF is highly heterogeneous, involving multifactorial pathological mechanisms including metabolic dysregulation, inflammation, myocardial fibrosis, ventricular hypertrophy, and microvascular dysfunction.[30, 31, 32, 33, 34, 35, 36, 37, 38, 39] To address this complexity, the present study investigates the regulatory role of hepatic AGT in HFpEF through the above‐mentioned pathological axes:. Here, AGT is linked to cardiac hypertrophy.