AGT and cardiac hypertrophy: HFpEF involves multiple pathophysiological changes, including metabolic stress, cardiac hypertrophy, cardiac fibrosis, cardiac inflammation, and microvascular dysfunction.[30, 31, 32, 33, 34, 35, 36, 37, 38, 39] The current study systematically investigated the impact of hepatic AGT knockout on these pathological pathways and revealed novel mechanistic insights into hepatic AGT‐driven HFpEF pathogenesis.