Zinc-alpha2-glycoprotein modulates blood pressure by regulating renal lipid metabolism reprogramming - mediated urinary Na+ excretion in hypertension.

Deficiency of Azgp1 increased the malonyl CoA-mediated inhibition of CPT1 activity, leading to renal lipid metabolism reprogramming, resulting in accumulated fatty acids and increased NHE activity, subsequently decreasing urinary Na+ excretion and causing hypertension. These findings may provide a potential kidney-targeted therapy in the prevention and treatment of hypertension.