Akr1c18, which codes for 20α-hydroxysteroid dehydrogenase, is an enzyme-encoding gene. It is involved in multiple biological processes related to steroid metabolism. For instance, it catalyzes the conversion of progesterone into 20α-hydroxyprogesterone and the reduction of PGH2 to PGF2α. It participates in pathways like parturition and is associated with the regulation of steroid hormones, thus having overall biological importance in reproduction-related functions. Mouse models have been crucial in studying Akr1c18's functions [1-10].

In gene-knockout (KO) mouse models, deletion of Mamld1 led to reduced Akr1c18 expression, defective functional luteolysis, parturition failure, and neonatal deaths, highlighting its role in labour initiation [2]. In Fndc5 mutant mice (lacking irisin), reduced Akr1c18 expression was associated with decreased fertility, irregular estrus, and disordered steroid hormone production [3]. PXR deficiency in mice induced Akr1c18 expression, promoting hepatocarcinogenesis, suggesting its role in liver tumor development [1]. Also, conditional deletion of Gα(q/11) from granulosa/luteal cells in mice prevented PGF2α-induced Akr1c18 expression, impairing parturition due to the inability to withdraw progesterone at the end of pregnancy [4].

In conclusion, Akr1c18 is essential for parturition, fertility-related steroid hormone regulation, and may play a role in hepatocarcinogenesis. Mouse KO models have been instrumental in revealing these functions, providing insights into reproductive biology and liver-related disease mechanisms, which may help in developing new strategies for treating related disorders.