Abstract
Transferrin is a plasma protein with the primary role of transporting iron through the body and delivering it to the cells that utilize it. Because free ionic iron is very toxic by creating free radicals, the importance of transferrin lies in its antioxidant properties. Atherosclerosis, a pathological process affecting arterial walls, is a chronic inflammatory response in which oxidative stress caused by free radicals is a key factor in its pathogenesis. We postulate therefore that the plasma protein transferrin acts protectively in these events, by holding iron in containment and reducing oxidative stress. Furthermore, it is possible that a disturbance in transferrin function and homeostasis is a direct factor triggering and exacerbating atherosclerosis. Decreased transferrin levels, increased transferrin saturation, defective transferrin binding of iron, or other disorders may lead to increased oxidative stress and lipid peroxidation involved in the pathology of atherosclerosis. Some oxidative stress-related diseases have been linked to such systemic transferrin abnormalities, and we hypothesize that similar disruptions could account for an unfavorable microenviroment in the evolvement of atherosclerotic plaques. If confirmed, this proposed mechanism would significantly improve our understanding of the disease.
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