Beth Israel Deaconess Medical Center, Department of Neurology, Division of Stroke & Cerebrovascular Disease, Harvard Medical School, 330 Brookline Avenue - Palmer 127, Boston, MA, 02215, USA.
Cerebrovascular Center, Cleveland Clinic, Cleveland, OH, USA.
Curr Cardiol Rep. 2019 Mar 4;21(4):20. doi: 10.1007/s11886-019-1106-z.
To discuss the mechanisms of iron regulation in the brain and the pathophysiological role of deregulation of iron homeostasis following a stroke, and to review existing evidence supporting the potential role of iron chelators in the treatment of ischemic and hemorrhagic stroke.
In recent years, accumulating evidence has highlighted the role of neuroinflammation in neurological injury after ischemic and hemorrhagic stroke, and that free iron is central to this process. Via the Fenton reaction, free iron catalyzes the conversion of superoxide ion and hydrogen peroxide into hydroxyl radicals, which promote oxidative stress. Advances in our understanding of changes in brain iron metabolism and its relationship to neuronal injury in stroke could provide new therapeutic strategies to improve the outcome of stroke patients. Pharmacological agents targeting brain iron regulation hold promise as potentially effective treatments in both ischemic and hemorrhagic stroke.
探讨脑内铁调节的机制，以及卒中后铁稳态失调的病理生理作用，并综述现有的证据支持铁螯合剂在缺血性和出血性卒中治疗中的潜在作用。
近年来，越来越多的证据强调了神经炎症在缺血性和出血性卒中性神经损伤中的作用，并且游离铁在这一过程中起核心作用。通过芬顿反应，游离铁催化超氧阴离子和过氧化氢转化为羟自由基，促进氧化应激。我们对卒中后脑铁代谢变化及其与神经元损伤关系的理解的进展，可能为改善卒中患者的预后提供新的治疗策略。针对脑铁调节的药物具有作为潜在有效治疗剂应用于缺血性和出血性卒中的前景。
