Conversely, administration of Fn1 inhibitor RGDS to mice remarkably ameliorated I/R-induced myocardial infarct size, myocyte apoptosis, inflammation, oxidative stress, and fibrosis, which were associated with inhibition of AMP/ATP-LKB1-AMPK-dependent mechanisms (Figure 7). Here, FN1 is linked to myocardial infarction.