Ptafr, the platelet-activating factor receptor, is a key component in various biological processes. Platelet-activating factor (PAF) is a phospholipid-derived inflammatory mediator, and Ptafr is involved in PAF-related pathways. Ptafr has pro-inflammatory, pro-coagulant, and angiogenic actions on the vasculature [5]. It is also associated with processes like cell proliferation, fibrosis, and metastasis, highlighting its overall biological importance [1,3,4,6]. Genetic models, such as gene knockout models, can be valuable for studying its functions.

In a TP53/CDKN2A double-knockout gastroesophageal junction organoid model, abrogation of PTAFR by siRNA knockdown or a pharmacologic inhibitor reduced proliferation and proneoplastic features in vitro and tumor formation in vivo. Mechanistically, FOXM1 activated PTAFR transcription by binding to its promoter, amplifying the PTAF-PTAFR pathway [1]. In a mouse model of atherosclerosis, PTAFR was identified as a key gene influencing the progression and prognosis of the disease, regulating neutrophil extracellular traps (NETs) formation [2]. In cardiac fibrosis models, knockdown of PTAFR affected pro-fibrotic collagen production mediated by the lncRNA PFL, and overexpression of PTAFR led to collagen production [3]. In a post-myocardial infarction cardiac fibrosis model, miR-30b-5p and miR-22-3p restrained fibrogenesis by targeting PTAFR [4].

In conclusion, Ptafr plays essential roles in processes like tumorigenesis, atherosclerosis, and cardiac fibrosis. Gene knockout-based research in these areas has revealed that Ptafr is a potential therapeutic target. In tumorigenesis, its inhibition can reduce cancer-promoting features; in atherosclerosis, it impacts disease progression; and in cardiac fibrosis, it is involved in collagen production. Understanding Ptafr's functions through these models provides insights into disease mechanisms and potential treatment strategies.