The major findings from this study include the following: (1) SRC-3 expression was increased in mouse hearts subjected to CIH, (2) SRC-3 KO ameliorated CIH-induced pathological changes, including cardiac hypertrophy, and (3) mechanistically, SRC-3 KO attenuated CIH-induced apoptosis and changes in the activity of a number of oxidative stress-related enzymes and inflammatory genes in the mouse hearts. This evidence concerns the gene NCOA3 and cardiac hypertrophy.