These researchers were able to reverse mitochondrial dysfunction in old cells by CRISPR inhibition of PUM2.
PUM2 expression increases upon aging and this facilitates the capture/trapping of Mff mRNA, either alone or in association with other RNA-binding proteins (RBPs) in ribonucleoprotein particles (RNP). Consequently, PUM2 prevents Mff translation, impairing mitochondrial fission and mitophagy thereby leading to mitochondrial dysfunction
This begs the question of whether there's another way to either inhibit PUM2 or increase Mff via small molecules (supplements).
Anyone have any insights?
