Cyp4a14, a member of the cytochrome P450 (Cyp450) enzyme superfamily, possesses NADPH monooxygenase activity and catalyzes omega-hydroxylation of medium-chain fatty acids and arachidonic acid. It is associated with lipid metabolism and oxidative stress, and is a target marker gene of PPARα [1,3,4].

In various disease models, Cyp4a14 has been shown to play important roles. In a study on non-alcoholic steatohepatitis (NASH), Schisandra lignans alleviated hepatic damage by regulating lipid metabolism-related enzymes including Cyp4a14 [2]. In diabetic nephropathy, silencing Cyp4a14 by siRNA inhibited the proliferation and fibrosis of mesangial cells [4]. Cyp4a14-knockout (KO) mice had a higher number of goblet cells in the colon and were more resistant to dextran sulfate sodium (DSS)-induced colitis, suggesting Cyp4a14-increased oxidative stress exacerbates DSS-induced colitis [5]. Also, disruption of Cyp4a14 in mice led to hypertension, driven by excessive fluid reabsorption in the proximal tubule secondary to overexpression of NHE3 [6].

In conclusion, Cyp4a14 is crucial in lipid metabolism, oxidative stress and related pathological processes. Studies using Cyp4a14 KO mouse models have revealed its roles in diseases such as NASH, diabetic nephropathy, colitis and hypertension, providing potential targets for treatment of these diseases.