Ptgs1, also known as prostaglandin-endoperoxide synthase 1 or cyclooxygenase (COX) 1, is a key enzyme in the biosynthesis of prostaglandins from arachidonic acid. It participates in maintaining normal physiological functions in the body, such as protecting the gastrointestinal mucosa, regulating platelet aggregation, and influencing vascular tone. The gene is involved in multiple biological pathways, and its activity is crucial for the balance of inflammation, cell growth, and tissue repair [1].

In the context of disease, in prostate cancer, androgen deprivation-induced ZBTB46-PTGS1 signaling promotes neuroendocrine differentiation [2]. In chronic myeloid leukemia, the proto-oncogene EVI1 upregulates PTGS1, reducing the action of tyrosine kinase inhibitors [3]. In non-small cell lung cancer, dihydroartemisinin, a potential PTGS1 inhibitor, potentiates cisplatin-induced cell death [4]. For osteoporosis and benign breast tumors in Korean women, PTGS1 gene variants are associated with these phenotypes and are modulated by ovariectomy [5]. In Chinese patients with ischemic stroke treated with aspirin, PTGS1 rs10306114 polymorphisms are related to stroke recurrence [6]. In Chinese Han stroke patients with aspirin therapy, PTGS1 polymorphisms interact with smoking to affect functional outcomes [7].

In conclusion, Ptgs1 is essential for normal physiological functions and is intricately involved in various disease processes. Research on Ptgs1, including through genetic models, has provided insights into its role in diseases such as cancer, leukemia, stroke, and osteoporosis, offering potential therapeutic targets for these conditions.