Endothelial dysfunction, a common feature of various cardiovascular diseases, is closely associated with the overexpression of reactive oxygen species (ROS)/reactive nitrogen species (RNS). The reaction between superoxide anion and nitric oxide (NO) can generate peroxynitrite with stronger oxidation ability, which can deplete NO by oxidizing various proteins, leading to endothelial contraction and relaxation dysfunction, and playing an important role in various cardiovascular diseases. This article reviews the pathways through which nitrosylation modified proteins are produced and the possible mechanisms by which they promote endothelial dysfunction in cardiovascular disease. It discusses the relationship between ROS/RNS mediated nitrosylation modification and endothelial dysfunction, which together promote the progression of cardiovascular disease. The article also discusses the application of therapeutic strategies such as clearing peroxynitrite, inhibiting ROS production pathways, and directly enhancing endothelial cell function in cardiovascular diseases related to endothelial dysfunction, which can provide reference for further research on the role of protein nitration modification as a post-translational intervention target in cardiovascular diseases.