Second, although PPARγ and PGC1α have been identified as potential targets for the protective effects of NOB against pathological cardiac remodeling after MI and we have initially verified that Nrf2/HO-1 could be the potential downstream effectors of PPARγ in the protective process, the interaction between them and whether other downstream effectors exist are worth further investigation. This evidence concerns the gene PPARGC1A and myocardial infarction.