Crot, short for Carnitine O-octanoyltransferase, is a peroxisomal enzyme involved in liver fatty acid oxidation [1,2]. It has also been associated with pathways related to vascular calcification, lipid metabolism, and potentially the TGF-β signaling pathway in ovarian cancer [2,3]. Genetic models, such as knockout mice, have been crucial in understanding its functions.

In Crot-deficient (Crot-/-) mice, metabolomic analysis showed increased levels of omega-3 fatty acids like EPA, DPA, and DHA in the liver, and EPA in the plasma. Also, anti-inflammatory dicarboxylic acids were higher in the plasma of Crot-/-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 promotes vascular calcification via fatty acid metabolism and mitochondrial dysfunction [2].

In conclusion, Crot plays a role in fatty acid metabolism and is involved in processes related to vascular calcification. The study of Crot-deficient mouse models has provided insights into its function in these disease-relevant processes, suggesting Crot inhibition could be a potential antifibrocalcific therapy [2].