TFAM and aortic aneurysm: As Tfam controls the transcription, replication, and stability of mitochondrial DNA (mtDNA),23 depleting Tfam has been proved to be an effective approach to induce severe mitochondrial dysfunction in different cells and tissues.24–27 Tfam-deficient VSMC mice developed aortic dilation, medial degeneration, aortic aneurysm, and fatal dissections, further supporting that mitochondrial function is a key regulator of the VSMC phenotype during aortic remodeling.