%20are%20deadly%20vascular%20disorders%20linked%20to%20genetic%20mutations%20such%20as%20ACTA2R179H%20and%20TGFBR2G357W,%20which%20disrupt%20vascular%20smooth%20muscle%20cell%20(VSMC)%20function.%20Th...){kind=link}
Nicotinamide Riboside Restores Mitochondrial Function in Aortic Aneurysms: Preclinical Findings
Synopsis
Thoracic aortic aneurysms (TAA) are deadly vascular disorders linked to genetic mutations such as ACTA2R179H and TGFBR2G357W, which disrupt vascular smooth muscle cell (VSMC) function. This study found that these mutations cause mitochondrial dysfunction, marked by reduced Mitochondrial Transcription Factor A (Tfam) expression, lower mitochondrial DNA, and impaired oxidative phosphorylation, forcing cells to rely on glycolysis. Treatment with nicotinamide riboside (NR), a vitamin B3–derived NAD+ precursor, restored mitochondrial respiration, increased Tfam and mtDNA levels, and promoted a healthy, contractile VSMC phenotype by improving actin polymerization and reducing matrix metalloproteinase activity. These results reveal mitochondrial dysfunction as a key factor in hereditary TAAs and identify NR and other mitochondrial boosters as promising therapeutic strategies to maintain aortic integrity and prevent aneurysm progression.
Journal
Cells