Cyp1a1, a cytochrome P450 enzyme, is regulated by the aryl hydrocarbon receptor (AHR) signaling pathway [3]. It plays a crucial role in the metabolism of polycyclic hydrocarbons in the environment and is associated with the metabolism of pro-carcinogenic compounds into highly carcinogenic metabolites [1,3]. Additionally, it has gained significance in drug metabolism, mediating drug-drug interactions, and bioactivation of prodrugs [3]. Gene-targeted mice can serve as a valuable model system to study its in vivo function as a host factor determinant of environmentally-caused cancers in humans [1].

Mice constitutively expressing Cyp1a1 showed increased CYP1A1 enzymatic activity in the skin, leading to exacerbated immune cell activation and skin pathology, similar to Ahr-deficient mice. Inhibition of CYP1A1 enzymatic activity improved skin immunopathology by restoring beneficial AHR signaling, suggesting that dysregulation of the AHR/CYP1A1 axis may be involved in inflammatory skin disease [2]. PM2.5 exposure in mice led to adverse pregnancy outcomes through the KLF9/CYP1A1 transcriptional axis, as PM2.5 stimulated KLF9 to bind to the CYP1A1 promoter region, modulating downstream phenotypes related to oxidative stress and mitochondrial apoptosis in trophoblasts [4].

In conclusion, Cyp1a1 is essential in metabolism, especially of environmental carcinogens, and drug-related processes. Mouse models have revealed its role in inflammatory skin disease and adverse pregnancy outcomes, providing insights into the underlying mechanisms and potential therapeutic targets in these disease areas.