During heart regeneration, the oxidative phosphorylation (OXPHOS) pathway was downregulated in wild-type cells, but upregulated (to inhibit cardiomyocyte proliferation) in Nrf1-cKO hearts, leading to a significant increase of ROS, along with upregulated expression of two cardiac stress markers Nppa and Nppb in the Nrf1-cKO MI hearts 382. This evidence concerns the gene NRF1 and myocardial infarction.