TFAM and myocardial infarction: Ikeuchi et al created transgenic mice that overexpress the human TFAM gene and found that overexpression of TFAM protected against MCN truncation in heart tissue and inhibited LV remodeling after myocardial infarction.[25] Mitochondria-encoded gene expression is largely regulated by the MCN.[14] A decrease in the MCN results in a corresponding decrease in mtRNA and proteins, and hence mitochondrial dysfunction.[26] Therefore, maintenance of a higher MCN is important to preserve mitochondrial function.