Pcyox1, short for 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]. This process is potentially related to multiple biological pathways and has overall biological importance in various physiological and pathological processes. Gene knockout (KO) mouse models have been valuable for studying its functions.

In KO mouse models, Pcyox1 -/- mice showed delayed in vivo thrombus formation after carotid artery injury and protection from collagen/epinephrine-induced thromboembolism. Deletion of Pcyox1 led to reduced platelet/leukocyte aggregates, platelet aggregation, alpha granules release, and αIIbβ3 integrin activation in response to agonists [1]. In adipogenesis studies, Pcyox1 -/-/Apoe -/- mice fed a high-fat diet had lower body weight due to reduced visceral adipose content, and Pcyox1 gene silencing prevented 3T3-L1 preadipocyte differentiation [2]. In atherosclerosis research, Pcyox1 deficiency in Apoe -/- mice retarded atheroprogression, decreased lesion vulnerability, and reduced plasma lipid levels and inflammation [3].

In conclusion, Pcyox1 plays crucial roles in thrombosis, adipogenesis, and atherosclerosis as revealed through KO mouse model-based research. Its absence leads to platelet hypo-reactivity, impaired arterial thrombosis, reduced adipogenesis, and retarded atheroprogression. These findings suggest Pcyox1 could be a potential target for drugs related to these disease areas.