Associated with this functional deficit, the hearts of the knockout mice are enlarged (hypertrophic) and present significant dysregulation in genes involved in cardiovascular disease, including genes critical for cardiac contractility (Ryr2; dystrophin, Dmd), repressing cardiac hypertrophy (Krüppel like factor 15, Klf15), promoting cardiomyocyte survival (prostaglandin D2 synthase, Ptgds) and inhibiting inflammation (lipocalin 2, Lcn2; tristetraprolin, Zfp36) [94]. This evidence concerns the gene PTGDS and cardiac hypertrophy.