Hyperhomocysteinemia, vascular pathology, and endothelial dysfunction.

摘要: Hyperhomocysteinemia has been associated with premature atherothrombotic vascular disease. It is not known whether hyperhomocysteinemia induces a distinct type of Its interaction, if any, traditional risk factors also remains unclear. The pathophysiological mechanisms linking to disease have extensively studied in vitro and animals. From these studies, it suggested that homocysteine limits the bioavailability nitric oxide (NO), increases oxidative stress, stimulates smooth cell proliferation, alters elastic wall properties. relevance proposed vivo unclear, because clinical studies yielded controversial results regard relation between plasma levels indices endothelial function, such as brachial artery flow-mediated vasodilatation endothelium-derived marker proteins. Up till now, there no controlled data on effects homocysteine-lowering treatment function or end points. precise (if any) by which mediates its adverse are fact unknown but may relate impaired muscle function.