Ptgis, also known as prostaglandin I2 synthase, is a member of the cytochrome P450 family. It catalyzes the isomerization of prostaglandin H2 to prostacyclin, a potent vasodilator and inhibitor of platelet aggregation [8]. PTGIS is involved in metabolic pathways, arachidonic acid metabolism, steroid biosynthesis, and cancer pathways [3]. It is also associated with fatty acid metabolism [2,6].

In patients with idiopathic pulmonary arterial hypertension (IPAH), rare loss-of-function variants in PTGIS were identified. These variants were associated with susceptibility to IPAH and a different pulmonary vascular response to iloprost stimulation [1]. In endometrial stromal cells, hypoxia-hindered methylation of PTGIS accelerates endometriosis progression by inducing CD16-NK-cell differentiation [4]. In prostate cancer, rsRNA-28S regulates chemoresistance by targeting PTGIS [5]. In endometrial cancer, PTGIS affects the malignant biological behavior of the cancer [6]. In lung squamous cell carcinoma, PTGIS promotes cancer cell proliferation, migration, and invasion [7]. In liver fibrosis, DNA methylation of PTGIS enhances hepatic stellate cells activation and liver fibrogenesis, while overexpression of PTGIS inhibits the activation of these cells and alleviates liver fibrosis [9]. In endothelial cells, nitric oxide-induced miR-199a/b downregulates PTGIS gene expression, leading to nitrovasodilator resistance [10].

In conclusion, Ptgis plays a crucial role in various physiological and pathological processes. Its function in prostacyclin synthesis affects vasodilation and platelet aggregation. Research on Ptgis using different models has revealed its associations with multiple diseases, including IPAH, endometriosis, prostate cancer, endometrial cancer, lung squamous cell carcinoma, liver fibrosis, and nitrovasodilator resistance. Understanding the role of Ptgis can provide insights into disease mechanisms and potential therapeutic targets.