Iron Neurotoxicity and Protection by Deferoxamine in Intracerebral Hemorrhage

Frontiers in Molecular Neuroscience

Voon Wee Yong³  Ruiyi Zhang⁴  Ruixue Wei⁴  Zhe Li⁴  Yan Zhang⁴  Yang Liu⁴  Suliman Khan⁴  Mengzhou Xue⁴ 

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

关键词: intracerebral hemorrhage;    brain edema;    deferoxamine;    iron overload;    neuronal death;   

DOI  :  10.3389/fnmol.2022.927334

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown