Agtr1a, which encodes the angiotensin II type 1a receptor (AT1aR), is a key gene in the renin-angiotensin system (RAS). The RAS is involved in cardiovascular control, hydromineral balance, and the neuroendocrine control of energy balance. AT1aR is a crucial mediator in the RAS, through which angiotensin II exerts its physiological effects [1,2,3,4,6].

In animal studies, proximal tubule-specific deletion of Agtr1a in mice (PT-Agtr1a-/-mice) attenuates circulating and intratubular angiotensin II-induced hypertension, indicating the gene's role in hypertension development [5]. Agtr1a-/-mice with experimental autoimmune myocarditis show reduced fibrosis and better systolic function, suggesting that Agtr1a-encoded ATR1 signaling in the bone marrow compartment is critical for cardiac fibrosis [8]. Also, in Agtr1a-/-mice infused with aldosterone, vascular remodeling, endothelial dysfunction, and enhanced fibronectin and collagen deposition are not observed as in wild-type mice, highlighting the requirement of functional Agtr1a-encoded AGTR1a for these vascular effects [7].

In conclusion, Agtr1a plays a vital role in multiple physiological and pathological processes, especially in hypertension, cardiac fibrosis, and vascular remodeling. The use of Agtr1a knockout (KO) and conditional knockout (CKO) mouse models has significantly enhanced our understanding of the gene's functions in these disease areas, providing valuable insights for potential therapeutic strategies.