JUN and heart failure: AP-1 binds to specific promoter elements in target genes to regulate mRNA expression in response to inflammatory stimuli.8 In the heart, AP-1 induces the deposition of collagen and the synthesis of endothelin-1, fibronectin, and transforming growth factor-β (TGF-β).4,7,9 By these means, AP-1 brings about modifications to the extracellular matrix and reduces cardiac contractility, inducing fibrosis of the interstitial substance and cardiomyocyte hypertrophy, eventually leading to heart failure.4