https://www.selleckchem.com/products/LBH-589.html
D-gal was found to trigger mitochondria damage, ROS production, and cell senescence in myocardial cells. The overexpression of Parkin or silencing of USP30 reduced D-gal-induced mitochondrial damage and relieved D-gal-induced myocardial cell senescence. Moreover, the in vivo experiments validated that either elevation of Parkin or silencing USP30 could alleviate D-gal-induced myocardial cell senescence in rats. Silencing USP30 alleviates D-gal-induced mitochondrial damage and consequently suppresses myocardial cell senescence by activat
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