Min Li

TL;DR: Melatonin exerts a hepatoprotective effect on mitochondrial-derived O2•−-stimulated autophagic cell death that is dependent on the SIRT3/SOD2 pathway, and is reported to protect against Cd-induced hepatotoxicity.

TL;DR: It is indicated that Cd induces mitochondrial loss via the overactivation of mitophagy following DNM1L-dependent mitochondrial fragmentation, and the balanced activity of D NM1L and mitophile signaling may be a potential therapeutic approach to treat Cd-induced hepatotoxicity.

TL;DR: The data suggest that QDs induced hepatocyte pyroptosis, liver inflammation and dysfunction via NLRP3 activation, which was caused by QDs-triggered mtROS production and Ca(2+) mobilization.

TL;DR: SIRT1 plays an essential role in the ability of moderate melatonin to stimulate PGC-1 alpha and improve mitochondrial biogenesis and function at least partially through melatonin receptors in cadmium-induced hepatotoxicity, which indicates that Sirtinol and SIRT1 siRNA each blocked the melatonin-mediated elevation in mitochondrial function.

TL;DR: This study shows some associations between MP use and inattention in Chinese adolescents, and suggests decreasing MP usage to less than 60 minutes per day may help adolescents to stay focused and centered.