Kdm8, also known as JMJD5, is a histone lysine demethylase/dioxygenase. It plays a crucial role in regulating various biological processes by demethylating H3K36me2. It is involved in cell cycle progression, cardiac metabolism, and tumor metabolism pathways, and is thus of great biological importance. Genetic models, such as KO/CKO mouse models, have been valuable in studying its functions [2,3,4,5].

In mouse cardiomyocytes, deletion of Kdm8 increased H3K36me2, activated Tbx15, and repressed target genes in the NAD+ pathway before the initiation of dilated cardiomyopathy. This led to the development of dilated cardiomyopathy and lethal heart failure, suggesting that Kdm8 maintains an active mitochondrial gene network by repressing Tbx15 to prevent this condition [1].

In conclusion, Kdm8 is essential in regulating cell cycle, cardiac metabolism, and potentially tumor-related processes. Mouse models, especially Kdm8 KO/CKO mouse models, have significantly contributed to understanding its role in preventing dilated cardiomyopathy, highlighting its importance in this disease area.