Glutaredoxin 2a Overexpression in Macrophages Promotes Mitochondrial Dysfunction but has Little or no Effect on Atherogenesis in LDL-Receptor Null Mice

摘要: Aims Reactive oxygen species (ROS)-mediated formation of mixed disulfides between critical cysteine residues in proteins and glutathione, a process referred to as protein S-glutathionylation, can lead loss enzymatic activity degradation. Since mitochondria are major source ROS number their susceptible protein-S-glutathionylation, we examined if overexpression mitochondrial thioltranferase glutaredoxin 2a (Grx2a) macrophages dyslipidemic atherosclerosis-prone mice would prevent dysfunction protect against atherosclerotic lesion formation.