Department of Pharmacology and Chemical Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA; UPMC Hillman Cancer Center, University of Pittsburgh, PA 15213, USA.
Trends Endocrinol Metab. 2019 Sep;30(9):575-577. doi: 10.1016/j.tem.2019.07.019. Epub 2019 Aug 6.
A recent study by Polyzos et al. (Cell Metab., 2019) shows that astrocytes in a Huntington disease (HD) mouse model switch from glycolysis to fatty acid oxidation (FAO), causing increased superoxide radical anion production and loss of succinate dehydrogenase (SD) activity. Blocking mitochondria reactive oxygen species (ROS) with an antioxidant compound called XJB-5-151 reversed lipofuscin formation and protected the mice.
最近,Polyzos 等人的一项研究(Cell Metab.,2019)表明,亨廷顿病(HD)小鼠模型中的星形胶质细胞从糖酵解转变为脂肪酸氧化(FAO),导致超氧阴离子自由基产生增加和琥珀酸脱氢酶(SD)活性丧失。一种名为 XJB-5-151 的抗氧化化合物阻断线粒体活性氧(ROS)可逆转脂褐素形成并保护小鼠。