Papel del Factor de Crecimiento Derivado de Plaquetas C (PDGF-CC) sobre mecanismos celulares asociados a un modelo de disfunción endotelial inducida por alta concentración de D-glucosa

Abstract

Loss of endothelial function is a common feature to all cardiovascular diseases 38 (CVDs). One of the risk factors associated with the development of CVD is the abnormal 39 increase in plasma glucose levels (hyperglycaemia) that occurs in patients with metabolic 40 disorders such as Type I and Type II Diabetes. Hyperglycaemia causes endothelial 41 dysfunction through increased production of reactive oxygen species (ROS) from different 42 cellular sources leading to oxidative stress. Vascular endothelial growth factor (VEGF) is 43 essential in the stimulation and maintenance of endothelial functional aspects and, although 44 it can mitigate the impact of ROS, VEGF-mediated signalling is partially inhibited in 45 diabetes. Therefore, the search for therapeutic strategies that preserve, protect and/or 46 improve the functions of the endothelium is of great relevance in the investigation of CVDs 47 associated with hyperglycaemia. Platelet-derived growth factor C (PDGF-CC) is a peptide 48 with angiogenic properties, independent of VEGF, that stimulates angiogenesis and 49 revascularization of ischemic tissue. In a diabetic mouse model, it stimulates mature 50 endothelial cell migration, angiogenesis, endothelial progenitor cell mobilization, and 51 increased neovascularization; protects blood vessels in a retinal degeneration model and 52 activates important signalling pathways in antiapoptosis and proliferation in endothelial cell 53 models. Consequently, the aim of this review is to update the information on the damage 54 that high glucose levels produce on endothelial function and the beneficial effects that 55 PDGF-CC could exert in this condition.