CYP7B1, a cytochrome P450 enzyme, hydroxylates carbons 6 and 7 of the B ring of oxysterols and steroids. This action reduces substrate biological activity and aids their conversion into excretable end-products. It is involved in cholesterol metabolism, especially in inactivating oxysterols and converting them to bile salts in the liver [1].

In KO mouse models, CYP7B1 deficiency attenuates experimental autoimmune encephalomyelitis, reducing leukocyte infiltration, suppressing pathogenic CD4+ T cell proliferation, and decreasing myeloid cell activation in the central nervous system [2]. In Cyp7b1-/-mice, cold-induced BAT-mediated clearance of fatty acids from triglyceride-rich lipoproteins is reduced, along with compromised BAT function and reduced fecal bile acid levels [4]. BM-MSCs from CYP7B1 conditional knockout mice have impaired activation abilities, related to delayed bone defect healing [3].

In conclusion, CYP7B1 is crucial for cholesterol metabolism, with its deficiency influencing multiple biological processes. The study of CYP7B1 KO/CKO mouse models has provided insights into its role in diseases such as neuroinflammatory diseases, cold-induced lipoprotein clearance, and stem cell activation, highlighting its potential as a therapeutic target in these areas.