Abstract
Blood lipids, particularly total and LDL cholesterol levels, are associated with all subtypes of brain infarction. Furthermore, many of the effects of elevated or modified low density lipoproteins on endothelial cells and endothelial cell processes could be expected to contribute to the development of atherosclerosis and therefore, to the association between lipids and atherosclerotic, particularly coronary and cerebrovascular disease. However, the extent to which “endothelial dysfunction” accounts for the known relationships between serum lipid concentrations, ischemic disease and endothelial progenitor cell (EPC) pathophysiology is yet to be established. On the basis of the mentioned and other reports, we hypothesize that higher levels of plasma LDL cholesterol not only directly impair endothelial cells, but also effect EPC number and function at the same time, thus influencing the endothelial repair process and disturbing the balance between the magnitude of injury and the capacity for repair, which leads to endothelial dysfunction and promotes the progression of stroke. Because EPCs have been implicated in various events requiring endothelialization, we further hypothesized that LDL-C could influence the action of EPCs and sensory neurons and that this could be important to know how LDL-C effects repair, injury and vasculoprotection . In order to corroborate this proposal, quantification is required for EPCs and DRG neurons treated with various concentrations of LDL-C and characterizing the underlying molecular mechanisms. The relative contributions of apoptotic and necrotic death to ischemia-induced neuronal loss may provide us information for understanding the underlying mechanisms. Conclusively, the aggressive management of risk factors, like cholesterol, could have a significant and positive impact on the natural history of atherosclerotic cerebrovascular disease.
