Cyp2j9, a member of the cytochrome P450 CYP2J subfamily, is an arachidonic acid omega-1 hydroxylase. It metabolizes arachidonic acid to 19-hydroxyeicosatetraenoic acid (19-HETE) [2]. This gene is highly expressed in the brain, liver, and lung, and is also expressed in mouse atrial HL-1 cells at a similar level to that in mouse hearts [2,4]. In the brain, it may play important functional roles as its product 19-HETE can inhibit the activity of P/Q-type Ca(2+) channels expressed in cerebellar Purkinje cells [2].

In lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice, the mRNA expression of Cyp2j9 was decreased [1]. This dysregulation of Cyp2j9, along with other CYPs/COX-2 metabolism changes of arachidonic acid, contributed to the uncontrolled inflammatory response in ALI [1]. In C57BL/6 mice, arsenic trioxide (ATO) induced Cyp2j9, which led to changes in the production of hydroxyeicosatetraenoic acids (HETEs), suggesting that ATO-induced hepatotoxicity may be related to the modification of bioactive AA metabolites by modulating Cyp2j9 and other CYPs [3].

In conclusion, Cyp2j9 plays a role in arachidonic acid metabolism and is involved in processes related to inflammation and potential toxicity. Studies in mouse models, such as those with LPS-induced ALI and ATO treatment, have revealed its significance in these disease-related conditions, providing insights into how its dysregulation can contribute to pathophysiological processes.