Pcyox1, known as prenylcysteine oxidase 1, is an enzyme involved in the degradation of prenylated proteins. It hydrolyzes the thioether bond of prenylcysteines in the final step of prenylated protein degradation, releasing hydrogen peroxide, cysteine, and the isoprenoid aldehyde [4]. It is expressed in different tissues such as vascular and blood cells, adipose tissue, liver, gastrointestinal tract, kidney, male reproductive tissue, and muscle [4].

Pcyox1 -/- mice have shown significant phenotypes. In thrombosis studies, FeCl3-induced carotid artery thrombus formation was delayed, and these mice were protected from collagen/epinephrine-induced thromboembolism. Pcyox1 deletion reduced platelet/leukocyte aggregates, platelet aggregation, alpha-granules release, and αIIbβ3 integrin activation in response to agonists [1]. In adipogenesis, Pcyox1 -/-/Apoe -/- mice on a high-fat diet had lower body weight due to reduced visceral adipose content. Pcyox1 gene silencing in 3T3-L1 preadipocytes prevented their differentiation, acting as an upstream regulator of key adipogenic players like FABP4, PPARγ, and C/EBPα [2]. In atherosclerosis, Pcyox1 deficiency in Apoe -/- mice retarded atheroprogression, decreased lesion vulnerability, reduced plasma lipid levels and inflammation [3].

In conclusion, Pcyox1 plays crucial roles in thrombosis, adipogenesis, and atherosclerosis. The use of Pcyox1 gene-knockout mouse models has revealed its functions in these biological processes and disease conditions, suggesting it could be a potential target for antithrombotic drugs and a key factor in understanding adipogenesis and atherosclerosis [1,2,3].