Preclinical models of pressure overload-induced LVH and CKD-induced cardiac remodelling consistently implicate renalase in the processes of cardiac hypertrophy and fibrosis, with its modulation (either genetically or via recombinant protein) affecting key signalling pathways like p38 and ERK1/2, and altering ECM deposition. This evidence concerns the gene MAPK3 and cardiac hypertrophy.