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Iron-mediated cardiovascular injury
1Division of Cardiology, University of Colorado Health Sciences Center, Denver 80262, USA.
Insights
Iron overload contributes to heart disease, but iron depletion may prevent conditions like reperfusion injury and atherosclerosis. Iron chelation shows promise for cardiovascular health.
Area of Science:
- Cardiovascular Science
- Hematology
- Cellular Biology
Background:
- Iron is vital for cellular function but can be detrimental in cardiac conditions.
- Pathologic roles of iron include reperfusion injury, hemochromatosis, beta-thalassemia, and coronary atherosclerosis.
- Anthracycline cardiotoxicity also involves iron's role in cellular injury.
Purpose of the Study:
- To review the mechanisms of iron's contribution to cardiovascular pathophysiology.
- To examine evidence supporting iron depletion for preventing cardiovascular diseases.
- To explore the potential of iron chelation in treating restenosis and atherogenesis.
Main Methods:
- Review of existing literature on iron metabolism and cardiovascular disease.
- Analysis of cell culture, isolated organ, and animal studies.
- Examination of clinical evidence for iron removal therapies.
Main Results:
- Iron overload states and normal iron stores contribute to cardiovascular pathophysiology.
- Phlebotomy and chelation therapy are established treatments for iron overload disorders.
- Studies suggest iron depletion may prevent reperfusion injury, restenosis, and atherogenesis.
Conclusions:
- Iron plays a dual role in cardiovascular health, being essential but also pathogenic in excess.
- Iron chelation is a potential therapeutic strategy for preventing cardiovascular events.
- Further research is warranted to fully elucidate iron's role and optimize chelation therapies.
Abstract:
Iron is an essential element for normal cellular function and general health. However, iron may play a pathologic role in certain cardiac conditions including reperfusion injury, hemochromatosis, beta-thalassemia and coronary atherosclerosis. It also may play a role in injury due to anthracycline cardiotoxicity. Removal of iron via phlebotomy for hemochromatosis and chelation therapy for beta-thalassemia are proven treatments. Cell culture, and isolated organ and animal studies suggest that depleting iron stores may prevent reperfusion injury, restenosis and even atherogenesis. This article will review mechanisms by which iron overload states and normal iron stores contribute to cardiovascular pathophysiology and the accumulating evidence that iron chelation may prevent restenosis and atherogenesis.