Iron In Arterial Plaque

Iron in arterial plaque: A modifiable risk factor for atherosclerosis.
Sullivan JL
Biochim Biophys Acta 2008 Jun 19.

It has been proposed that iron depletion protects against
cardiovascular disease. There is increasing evidence that one
mechanism for this protection may involve a reduction in iron levels
within atherosclerotic plaque. Large increases in iron concentration
are seen in human atherosclerotic lesions in comparison to levels in
healthy arterial tissue. In animal models, depletion of lesion iron
levels in vivo by phlebotomy, systemic iron chelation treatment or
dietary iron restriction reduces lesion size and/or increases plaque
stability. A number of factors associated with increased arterial
disease or increased cardiovascular events is also associated with
increased plaque iron. In rats, infusion of angiotensin II increases
ferritin levels and arterial thickness which are reversed by treatment
with the iron chelator deferoxamine. In humans, a polymorphism for
haptoglobin associated with increased cardiovascular disease is also
characterized by increased lesional iron. Heme oxygenase 1 (HO1) is an
important component of the system for mobilization of iron from
macrophages. Human HO1 promoter polymorphisms causing weaker
upregulation of the enzyme are associated with increased
cardiovascular disease and increased serum ferritin. Increased
cardiovascular disease associated with inflammation may be in part
caused by elevated hepcidin levels that promote retention of iron
within plaque macrophages. Defective retention of iron within arterial
macrophages in genetic hemochromatosis may explain why there is little
evidence of increased atherosclerosis in this disorder despite
systemic iron overload. The reviewed findings support the concept that
arterial plaque iron is a modifiable risk factor for atherogenesis.

Biochimica et biophysica acta [Biochim Biophys Acta]

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Iron In Arterial Plaque
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