Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke

Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the involved mechanisms in order to prevent or efficiently treat these injuries. What we know so far is that oxidative stress and mitochondrial dysfunction are significantly involved in the pathogenesis of ischemia/reperfusion injury. However, despite promising results obtained in experimental research, clinical studies trying to interfere with the oxidative pathways have mostly failed. The current article discusses the main mechanisms leading to ischemia/reperfusion injuries, such as mitochondrial dysfunction, excitotoxicity, and oxidative stress, and reviews the clinical trials with antioxidant molecules highlighting recent developments and future strategies.

Automated summary

This article discusses the application of recanalization therapy in the treatment of acute ischemic stroke and the potential ischemia/reperfusion injuries it may cause. Oxidative stress and mitochondrial dysfunction have been identified as significant factors in the pathogenesis of these injuries, but clinical studies targeting oxidative pathways have mostly been unsuccessful.