Iron Deficiency as a Therapeutic Target in Cardiovascular Disease

被引:14
作者
Lakhal-Littleton, Samira [1 ]
机构
[1] Univ Oxford, Dept Physiol Anat & Genet, Parks Rd, Oxford OX1 3PT, England
关键词
iron; hepcidin; iron regulatory proteins; cardiomyocyte; chronic heart failure; pulmonary arterial smooth muscle cells; pulmonary arterial hypertension; PULMONARY ARTERIAL-HYPERTENSION; CHRONIC HEART-FAILURE; QUALITY-OF-LIFE; FERRIC CARBOXYMALTOSE; MYOCARDIAL-INFARCTION; EXERCISE CAPACITY; ANEMIA; HOMEOSTASIS; PREVALENCE; CARDIOMYOPATHY;
D O I
10.3390/ph12030125
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Iron deficiency is the most common nutritional disorder in the world. It is prevalent amongst patients with cardiovascular disease, in whom it is associated with worse clinical outcomes. The benefits of iron supplementation have been established in chronic heart failure, but data on their effectiveness in other cardiovascular diseases are lacking or conflicting. Realising the potential of iron therapies in cardiovascular disease requires understanding of the mechanisms through which iron deficiency affects cardiovascular function, and the cell types in which such mechanisms operate. That understanding has been enhanced by recent insights into the roles of hepcidin and iron regulatory proteins (IRPs) in cellular iron homeostasis within cardiovascular cells. These studies identify intracellular iron deficiency within the cardiovascular tissue as an important contributor to the disease process, and present novel therapeutic strategies based on targeting the machinery of cellular iron homeostasis rather than direct iron supplementation. This review discusses these new insights and their wider implications for the treatment of cardiovascular diseases, focusing on two disease conditions: chronic heart failure and pulmonary arterial hypertension.
引用
收藏
页数:9
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