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Hepcidin Deficiency Protects Against Atherosclerosis.

Rajeev Malhotra1, Florian Wunderer2,3, Hanna J Barnes1

  • 1From the Cardiovascular Research Center and Cardiology Division of the Department of Medicine (R.M., H.J.B., M.D.B., C.L.S., H.S., D.K.R., K.D.B.), Massachusetts General Hospital and Harvard Medical School, Boston.

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Summary
This summary is machine-generated.

Hepcidin deficiency reduces iron in macrophages, decreasing inflammation and protecting against atherosclerosis in mice. This suggests targeting hepcidin may be a new treatment strategy for this disease.

Keywords:
atherosclerosishepcidinsinflammationironmacrophages

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Area of Science:

  • Cardiovascular Research
  • Iron Metabolism
  • Immunology

Background:

  • Inflammatory stimuli accelerate atherosclerosis.
  • Hepcidin, a regulator of iron homeostasis, increases with inflammation, trapping iron in macrophages.
  • The impact of macrophage iron on atherosclerosis is not fully understood.

Purpose of the Study:

  • To investigate the effects of hepcidin deficiency and reduced macrophage iron on atherosclerosis development.
  • To determine if reduced macrophage iron contributes to atherosclerosis protection in hepcidin-deficient mice.

Main Methods:

  • Mice lacking hepcidin and LDL receptors (Hamp-/-/Ldlr-/-) and controls (Hamp+/+/Ldlr-/-) were fed a high-fat diet for 21 weeks.
  • Iron dextran was administered to control mice to increase serum iron levels.
  • THP1 human macrophages were treated with an iron chelator in vitro to model hepcidin deficiency.

Main Results:

  • Hamp-/-/Ldlr-/- mice exhibited reduced aortic macrophage activity and atherosclerosis compared to controls.
  • Increased serum iron in control mice did not reduce atherosclerosis.
  • Macrophages from hepcidin-deficient mice had less iron and a less proinflammatory (M1) phenotype.
  • In vitro, iron chelation reduced M1 phenotype and oxidized LDL uptake in macrophages.

Conclusions:

  • Hepcidin deficiency in hyperlipidemic mice led to decreased macrophage iron, reduced inflammation, and protection from atherosclerosis.
  • Reducing hepcidin activity and subsequent macrophage iron may be a novel therapeutic approach for atherosclerosis.