Crot, short for Carnitine O-octanoyltransferase, is a well-established peroxisomal enzyme. It is involved in liver fatty acid oxidation, and recent research has explored its role in promoting vascular calcification. It also participates in lipid metabolism-related pathways, and its function is of great biological importance [1,2]. Genetic models, such as knockout mouse models, have been crucial for studying its functions.

In Crot-deficient (Crot-/-) mice, metabolomic analysis showed that omega-3 fatty acids like EPA, DPA, and DHA were increased in the liver, and EPA was higher in the plasma. Anti-inflammatory dicarboxylic acids were also elevated in the plasma of Crot-deficient mice, suggesting a potential anti-calcification mechanism of Crot suppression [1]. In addition, Nuclease technology-mediated Crot deficiency in LDL receptor-deficient mice reduced aortic and carotid artery calcification without affecting bone density or lipid levels in the liver and plasma, indicating Crot's role in vascular calcification via promoting fatty acid metabolism and mitochondrial dysfunction [2].

In conclusion, Crot is essential in liver fatty acid oxidation and lipid metabolism. Studies using Crot knockout mouse models have revealed its significant role in vascular calcification, suggesting that Crot inhibition may be a potential antifibrocalcific therapy. These models have provided valuable insights into the function of Crot in specific disease-related biological processes [1,2].