JNK1 knockout in the heart of mice resulted in elevated cardiac fibrosis when subjected to pressure overload,[136] whereas treatment of JNK inhibitor SP600125 to dilated cardiomyopathy in hamsters resulted in increased apoptosis and fibrosis.[111] Moreover, in aortic banded rats, treatment of all trans-retinoic acid to rats inhibit MAPK signalling, including the JNK pathway, via the upregulation of MKP-1/2, which in turn prevent the development of cardiac remodelling.[111] Indeed, the roles of MKP-1/2 have been widely associated with cardioprotective functions. Here, DUSP1 is linked to fibrosis.