Ch25h, or cholesterol 25-hydroxylase, is a key enzyme that converts cholesterol to 25-hydroxycholesterol (25HC), thereby playing a crucial role in cholesterol metabolism. This process is involved in various biological pathways, including immune responses, inflammation, and autophagy. Genetic models, such as gene knockout (KO) mouse models, are valuable tools for studying Ch25h's functions [1-10].

In KO mouse models, Ch25h deficiency has been associated with various outcomes. In osteoarthritis, knockout of Ch25h and CYP7B1 abrogated the pathogenesis, indicating their role in the disease [1]. In cerebral ischemic stroke, Ch25h-/-mice had significantly increased infarct volume, highlighting the neuroprotective role of CH25H+ microglia [2]. In non-alcoholic fatty liver disease (NAFLD), Ch25h knockout mice on a high-fat diet showed higher serum cholesterol and triglyceride levels and were prone to hepatic steatosis, suggesting Ch25h's importance in lipid metabolism and inflammation regulation [3].

In conclusion, Ch25h is essential in regulating cholesterol metabolism, immune responses, and inflammation. Studies using KO mouse models have revealed its significance in diseases like osteoarthritis, cerebral ischemic stroke, and NAFLD. Understanding Ch25h's functions provides insights into disease mechanisms and potential therapeutic targets for these conditions.