In summary, MK became upregulated during heart failure and seems to have a detrimental function in cardiac hypertrophy, heart failure related to TAC-induced pressure overload and chronic kidney disease as well as pediatric DMC, while it had a preserving, protective effect in tachycardia-associated heart failure, contributed to zebrafish heart regeneration and might be involved in PTPRZ1-dependent cardiac morphogenesis. This evidence concerns the gene PTPRZ1 and cardiac hypertrophy.