Ptger1, also known as the E-prostanoid 1 receptor (EP1), is a G-protein coupled receptor that binds prostaglandin E2 (PGE2). It is involved in multiple biological processes, with its activation influencing various signaling pathways, such as the PKC/Nrf2 cascade. Ptger1 has significance in physiological and pathologic conditions, including cardiac, renal, and immune-related processes [1,2,3].

In gene knockout studies, Ptger1 deletion in diabetic mouse models (streptozotocin and OVE26 models) attenuated renal injury. Albuminuria, mesangial matrix expansion, and glomerular hypertrophy were reduced compared to wild-type counterparts. In cultured podocytes, EP1 antagonism decreased angiotensin II-mediated superoxide generation, suggesting its role in podocyte-associated injury. Also, EP1 deletion reduced diabetes-induced expression of fibrotic markers in proximal tubule cells [2].

In conclusion, Ptger1 plays important roles in renal function during diabetes as revealed by gene knockout mouse models. Its activation seems to contribute to diabetic nephropathy progression in podocytes, proximal tubule, and the vasculature. Understanding Ptger1's function through such models provides insights into potential therapeutic strategies for diabetic nephropathy [2].