Tbxa2r, encoding the α isoform of the thromboxane receptor (TPα receptor), is a G protein-coupled receptor. It participates in tissue inflammation, platelet aggregation, and is involved in multiple signaling pathways relevant to various biological processes. Its biological importance lies in its role in thrombus formation, fibroblast activation, and susceptibility to different diseases [1,2].

In a study on pulmonary fibrosis, genetic deletion of Tbxa2r protected mice from bleomycin-induced lung fibrosis, suggesting that Tbxa2R signaling is crucial for fibrotic remodeling. F2-isoprostanes, elevated during fibrosis, induce Tbxa2R signaling in fibroblasts and mediate myofibroblast activation, at least in part, via potentiation of TGF-β signaling [2]. In another study, a case-control study in Brazil found that carriers of certain Tbxa2r variant alleles (rs2238631.T and rs4807491.G) had a 3-to 4-fold increased risk of aspirin-induced upper gastrointestinal bleeding in patients with cardiovascular diseases treated with low-dose aspirin [3].

In conclusion, Tbxa2r is essential in processes like thrombus formation and fibroblast activation. Gene knockout models, such as in the study of pulmonary fibrosis, have revealed its significance in fibrotic remodeling. The role of Tbxa2r in diseases like pulmonary fibrosis and aspirin-induced upper gastrointestinal bleeding showcases its potential as a therapeutic target for these conditions.