Iron Neurotoxicity and Protection by Deferoxamine in Intracerebral Hemorrhage

Zhe Li; Yang Liu; Ruixue Wei; Suliman Khan; Ruiyi Zhang; Yan Zhang; Voon Wee Yong; Mengzhou Xue

doi:10.3389/fnmol.2022.927334

Iron Neurotoxicity and Protection by Deferoxamine in Intracerebral Hemorrhage

Front Mol Neurosci. 2022 Jun 16:15:927334. doi: 10.3389/fnmol.2022.927334. eCollection 2022.

Authors

Zhe Li^{1

2

3}, Yang Liu^{1

2

3}, Ruixue Wei^{1

2

3}, Suliman Khan^{1

2

3}, Ruiyi Zhang^{1

2

3}, Yan Zhang^{1

2

3}, Voon Wee Yong⁴, Mengzhou Xue^{1

2

3}

Affiliations

¹ Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
² Academy of Medical Science, Zhengzhou University, Zhengzhou, China.
³ Henan Medical Key Laboratory of Translational Cerebrovascular Diseases, Zhengzhou, China.
⁴ Department of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada.

Abstract

Intracerebral hemorrhage (ICH) is a subtype of stroke that is characterized by high morbidity and mortality, for which clinical outcome remains poor. An extensive literature indicates that the release of ferrous iron from ruptured erythrocytes in the hematoma is a key pathogenic factor in ICH-induced brain injury. Deferoxamine is an FDA-approved iron chelator that has the capacity to penetrate the blood-brain barrier after systemic administration and binds to iron. Previous animal studies have shown that deferoxamine attenuates ICH-induced brain edema, neuronal death, and neurological deficits. This review summarizes recent progress of the mechanisms by which deferoxamine may alleviate ICH and discusses further studies on its clinical utility.

Keywords: brain edema; deferoxamine; intracerebral hemorrhage; iron overload; neuronal death.

Publication types

Review