Moreover, SIRT3 modulates proinflammatory and profibrotic signals in cardiomyocytes via FOS/AP-1 pathways, whereas the SIRT3 knockout mice experienced significant myocardial fibrosis associated with increased activity of AP-1 transcriptional activity (178), implying that SIRT3 activation is a potential vehicle for treating cardiac fibrosis. This evidence concerns the gene JUN and Myocardial fibrosis.