Cyp2j5 is a gene encoding a cytochrome P450 enzyme. It is abundant in the mouse kidney and is active in metabolizing arachidonic acid to epoxyeicosatrienoic acids (EETs), which are involved in modulating sodium transport, vascular tone, and fluid/electrolyte transport [3,4,5]. It may also participate in the CYPs/cyclooxygenase-2 (COX-2) pathways related to inflammation [2].

Gene knockout studies on Cyp2j5 in mice have provided valuable insights. In Cyp2j5-/-mice, acetylcholine-induced relaxation was different from wild-type C57Bl/6 mice, and this relaxation in Cyp2j5-/-mice depended on nitric oxide (NO) but not CYP-epoxygenases. Also, angiotensin-II reduced acetylcholine-and NECA-induced relaxation in both Cyp2j5-/-and C57Bl/6 mice [1]. Female Cyp2j5-/-mice had increased blood pressure, enhanced proximal tubular transport rates, and exaggerated afferent arteriolar responses to angiotensin II and endothelin I, which could be restored to normal by estrogen replacement [5]. Additionally, in lipopolysaccharide-induced acute lung injury in mice, the mRNA expression of Cyp2j5 decreased, suggesting its role in the dysregulation of CYPs/COX-2 metabolism of ARA and the associated inflammatory response [2].

In conclusion, Cyp2j5 plays essential roles in physiological processes such as vascular relaxation, blood pressure regulation, and proximal tubular transport, with a sex-specific aspect related to estrogen. Its dysregulation is also associated with inflammatory conditions like acute lung injury. Studies using Cyp2j5 knockout mouse models have been crucial in uncovering these functions and their implications in disease-related processes.