Molecular pathophysiological mechanisms of ischemia/reperfusion injuries after recanalization therapy for acute ischemic stroke

With the larger variety of methods employed, recanalization therapy is increasingly used to treat acute ischemic stroke resulting in about one-third of patients undergoing early neurological deterioration, in which ischemia/reperfusion injuries are the main cause, leading to increases in the infarcted area, the no-reflow phenomenon, or hemorrhagic transformation. Efficient prevention or treatment of these injuries depends on extensive knowledge of the involved mechanisms. These pathways have dual, damaging, and neuroprotective effects, depending on the timing or protein subtype involved. The current article reviews the main mechanisms contributing to the pathophysiology of these injuries, such as mitochondrial dysfunction, cellular calcium overload, excitotoxicity, oxidative stress, apoptosis, and neuroinflammation.

Automated summary

Recanalization therapy, increasingly used for treating acute ischemic stroke, results in about one-third of patients experiencing early neurological deterioration due to ischemia/reperfusion injuries. Extensive knowledge of the involved mechanisms is crucial for efficient prevention or treatment of these injuries, which include mitochondrial dysfunction, cellular calcium overload, excitotoxicity, oxidative stress, apoptosis, and neuroinflammation. The pathways contributing to the pathophysiology of these injuries have dual effects, being damaging or neuroprotective depending on the timing or protein subtype involved.