Oxidized low-density lipoprotein (ox-LDL) can impair endothelial function and lead to the development of atherosclerosis. Protein S-nitrosylation is sensitive to the cellular redox state and acts as a crucial regulator and executor of NO signaling pathways. Aberrant S-nitrosylation contributes to the pathogenesis of cardiovascular and cerebrovascular diseases. However, the effect of ox-LDL on S-nitrosylation and its significance for endothelial dysfunction have not been studied at the S-nitrosylation proteome level. In our study, many key proteins belonged to ribosomal structure and translational regulatory proteins, covering the entire translation process. These results indicated that S-nitrosylation of the translational machinery in vascular endothelial cells was susceptible to ox-LDL.