Cyp2j5 is a cytochrome P450 enzyme that is abundant in the mouse kidney. It is active in the metabolism of arachidonic acid to epoxyeicosatrienoic acids (EETs), which are involved in modulating sodium transport, vascular tone, and fluid/electrolyte transport, as well as mediating hormonal action in the kidney [4]. It may also be associated with the metabolism of small molecules like flavanone, DHEA, and 7-ethoxycoumarin [6].

In Cyp2j5-/-mice, acetylcholine-induced relaxation was different from that in C57Bl/6 mice, and it depended on nitric oxide rather than CYP-epoxygenases. Angiotensin-II reduced acetylcholine-and NECA-induced relaxation in both Cyp2j5-/-and C57Bl/6 mice, and there was a gender-specific difference in NECA-induced response in Cyp2j5-/-mice when treated with Ang-II [1]. Female Cyp2j5-/-mice had increased blood pressure, enhanced proximal tubular transport rates, and exaggerated afferent arteriolar responses to angiotensin II and endothelin I, and these effects were related to reduced plasma 17β-estradiol levels [5]. Also, deletion of Cyp2j5 led to decreased EET production in the kidney [5]. In lipopolysaccharide-induced acute lung injury in mice, the mRNA expression of Cyp2j5 was decreased [2]. The renal expression of Cyp2j5 is up-regulated by androgen and down-regulated by estrogen [3].

In conclusion, Cyp2j5 plays crucial roles in the regulation of vascular relaxation, blood pressure, and proximal tubular function, with gender-specific differences. Its dysregulation is associated with conditions like acute lung injury. Gene knockout mouse models have been instrumental in revealing these functions of Cyp2j5 in the context of these biological processes and disease-related phenotypes [1,2,3,5].