RÉSUMÉ
Vascular calcification (VC), which is closely associated with significant mortality in cardiovascular disease, chronic kidney disease (CKD), and/or diabetes mellitus, is characterized by abnormal deposits of hydroxyapatite minerals in the arterial wall. The impact of oxidative stress (OS) on the onset and progression of VC has not been well described. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, xanthine oxidases, myeloperoxidase (MPO), nitric oxide synthases (NOSs), superoxide dismutase (SOD) and paraoxonases (PONs) are relevant factors that influence the production of reactive oxygen species (ROS). Furthermore, excess ROS-induced OS has emerged as a critical mediator promoting VC through several mechanisms, including phosphate balance, differentiation of vascular smooth muscle cells (VSMCs), inflammation, DNA damage, and extracellular matrix remodeling. Because OS is a significant regulator of VC, antioxidants may be considered as novel treatment options.
Sujet(s)
Muscles lisses vasculaires , Calcification vasculaire , Humains , Muscles lisses vasculaires/métabolisme , Myocytes du muscle lisse , NADPH oxidase , Stress oxydatif , Espèces réactives de l'oxygène/métabolisme , Calcification vasculaire/métabolismeRÉSUMÉ
Atherosclerosis (AS) is the pathophysiologic basis of many cardiovascular diseases. A number of studies have shown that post-translational modification (PTM) contributes to the initiation and progression of AS. For example, recent studies found that SUMOylation, ie, small ubiquitin-like modifier (SUMO) conjugation to target substrate proteins, was involved in AS. This PTM appears related to endothelial cell dysfunction (ECD), dyslipidemia and vascular smooth muscle cell (VSMC) proliferation. This review focuses on the molecular effects of SUMOylation in the initiation and progression of AS, including ECD, dyslipidemia and VSMC proliferation to better understand this pathologic process.
