Nicotinamide Riboside Helps Protect the Heart by Improving Mitochondrial Function: Preclinical Findings
Synopsis
Endothelial-to-mesenchymal transition (EndMT) contributes to heart scarring (cardiac fibrosis), but how it happens and how to treat it is not fully known. Researchers found that a process in mitochondria called the mitochondrial unfolded protein response (mtUPR) is important in EndMT caused by TGF-β1. TGF-β1 lowers mtUPR, but the NAD+ precursor nicotinamide riboside (NR) can restore mtUPR and reduce EndMT. NR works by regulating prohibitin proteins (PHB and PHB2). Blocking these proteins stops NR’s benefits, while increasing them helps protect mitochondria and reduce EndMT. In mice, NR also prevented EndMT caused by heart stress. This suggests NR could be a potential therapy to protect the heart from fibrosis.
Journal
The International Journal of Biochemistry & Cell Biology