In mouse and human models of pathological myocardial hypertrophy leading to cardiac dysfunction, ERK1/2, SAPK/JNK, and p38 MAPK are activated and increased in the heart, and these pathways further increase the expression of inflammatory mediators (TNF, IL-6) and hypertrophic factors (ET-1) [43]. Here, EDN1 is linked to cardiac hypertrophy.