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 and plays important roles in various biological processes. PGE2/PTGER1 axis can regulate anti-oxidative gene expression through the PKC/Nrf2 cascade, and is associated with processes like cell survival, ferroptosis regulation, and inflammation-related responses [1].

In diabetic mouse models, PTGER1 deletion attenuated renal injury, including albuminuria, mesangial matrix expansion, and glomerular hypertrophy. This indicates that PTGER1 activation contributes to the progression of diabetic nephropathy in podocytes, proximal tubules, and the vasculature [2]. In addition, maternal protein restriction during pregnancy led to a positive correlation between DNA hypermethylation of renal Ptger1 and its high mRNA expression in offspring, suggesting an epigenetic link to disease susceptibility [3,4].

In conclusion, Ptger1 is a crucial receptor in mediating PGE2-related biological functions. Studies using gene knockout mouse models have revealed its role in diabetic nephropathy and the impact of prenatal nutritional factors on its epigenetic regulation. These findings contribute to our understanding of the underlying mechanisms of related diseases and may provide potential therapeutic targets.