Ptger1, also known as the E-prostanoid 1 receptor, is a G-protein coupled receptor that binds prostaglandin E2 (PGE2). It is involved in multiple signaling pathways, such as the PKC/Nrf2 cascade, and plays significant roles in various biological processes and disease conditions [1].

In diabetic mouse models, PTGER1 deletion attenuated renal injury, including albuminuria, mesangial matrix expansion, and glomerular hypertrophy. EP1 antagonism also decreased angiotensin II-mediated superoxide generation in cultured podocytes, suggesting that PTGER1 activation contributes to diabetic nephropathy progression in podocytes, proximal tubule, and the vasculature [2]. In cardiomyocytes, genetic depletion of EP1 in mice worsened doxorubicin-induced cardiac injury, while EP1 activation protected cardiomyocytes from doxorubicin-induced ferroptosis by promoting Nrf2-driven anti-oxidative gene expression [1].

In conclusion, Ptger1 is crucial in processes like cardiac protection against ferroptosis and renal response in diabetes. Gene knockout mouse models have revealed its role in these disease areas, highlighting its potential as a therapeutic target for conditions such as diabetic nephropathy and doxorubicin-induced cardiomyopathy.