Molecular pathophysiological mechanisms of ischemia/reperfusion injuries after recanalization therapy for acute ischemic stroke
| Autor: | Ioana Adriana Ardelean, Anamaria Jurcau |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Mitochondrial Diseases Ischemia Excitotoxicity Neurosciences. Biological psychiatry. Neuropsychiatry Mitochondrion medicine.disease_cause Neuroprotection neuroinflammation Internal medicine Animals Humans Medicine oxidative stress Neuroinflammation Ischemic Stroke business.industry General Neuroscience apoptosis General Medicine medicine.disease reperfusion injury Pathophysiology mitochondria Neuroinflammatory Diseases Reperfusion Cardiology Calcium business Reperfusion injury excitotoxicity Oxidative stress RC321-571 |
| Zdroj: | Journal of Integrative Neuroscience, Vol 20, Iss 3, Pp 727-744 (2021) |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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