Ptgs2, also known as Prostaglandin-endoperoxide synthase 2 or Cyclooxygenase 2 (COX2), is the rate-limiting enzyme in the production of prostaglandins (PGs) [6]. It is involved in the PTGS2/COX2-PGE2 signaling cascade, which is associated with various physiological and pathophysiological processes, such as constriction or dilation of blood vessels, inflammation, pain, and fever [1].

In the context of multiple diseases, studies have revealed its significance. In atherosclerosis, PTGS2 was upregulated in advanced stages, and it might be the hub gene with its expression positively associated with the disease severity [2]. In type 1 diabetes mellitus, the PTGS2/COX2-PGE2 signaling cascade has controversial effects on pancreatic islet cells, being both a cause and consequence of inflammation [1]. In chronic spontaneous urticaria, PTGS2 may be a potential immune regulator, and its inhibition could be a new treatment perspective [5]. In colorectal cancer, PTGS2-positive patients had an increased risk of tumor recurrence and poorer cancer-specific survival [4]. Also, RUNX1-induced upregulation of PTGS2 promotes CRC cell growth, migration, and invasion [9]. In nasopharyngeal carcinoma, miR-26a-5p suppresses the progression by inhibiting PTGS2 expression [10]. In intervertebral disc degeneration, the ERBB2-PTGS2 axis is involved in regulating nucleus pulposus cell senescence [8]. In pulmonary fibrosis, ADAM17/PTGS2 promotes the disease by regulating ferroptosis in fibroblasts [7]. Endothelial ROBO4 can suppress PTGS2/COX-2 expression and associated inflammatory diseases [3].

In conclusion, Ptgs2 is a crucial gene in the production of prostaglandins and is involved in multiple disease-related processes. Studies, including those using potential gene-knockout models in the context of various diseases like atherosclerosis, diabetes, cancer, and inflammatory skin and lung diseases, have helped in understanding its role, providing insights into possible therapeutic strategies targeting Ptgs2 in these disease areas.