PPARGC1A and ischemic cardiomyopathy: The observation that EET-agonist increases mitochondrial fusion and decreases mitochondrial fission supports the contention that HO activity is mediated by PGC-1α, and is consistent with prior observations that increased HO-1 levels, as well as CO-releasing molecules, exert cardio-protective, anti-fibrotic, and anti-apoptotic effects in both ischemic and non-ischemic cardiomyopathy [46,50].