Further studies are needed to investigate whether elevated 4-HNE can cause the overexpression of matrix metalloproteinases through activation of the NF-kB pathway or promote oxidative stress-induced cardiomyocyte apoptosis or autophagy via either the MAPK or PI3K/Akt/mTOR signaling pathways in atrial tissue, as previously reported in other cardiovascular disease models [42,43,44]. Here, MTOR is linked to cardiovascular disorder.