IMR Press / JIN / Volume 20 / Issue 3 / DOI: 10.31083/j.jin2003078
Open Access Review
Molecular pathophysiological mechanisms of ischemia/reperfusion injuries after recanalization therapy for acute ischemic stroke
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1 Psycho-neurosciences and Rehabilitation Department, Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Bihor, Romania
2 Neurology Department, Clinical Municipal Hospital Oradea, 410154 Oradea, Bihor, Romania
3 Physiopathology Department, Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Bihor, Romania
4 Cardiology Department, Clinical Emergency County Hospital Oradea, 410169 Oradea, Bihor, Romania
J. Integr. Neurosci. 2021, 20(3), 727–744; https://doi.org/10.31083/j.jin2003078
Submitted: 3 June 2021 | Revised: 28 June 2021 | Accepted: 15 July 2021 | Published: 30 September 2021
Abstract

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.

Keywords
Reperfusion injury
Excitotoxicity
Mitochondria
Oxidative stress
Apoptosis
Neuroinflammation
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