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. 2019 Sep 11;20(18):4500. doi: 10.3390/ijms20184500

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Role of 20-HETE in the progression of ischemic and hemorrhagic strokes. Ischemic stroke leads to hypoxia and ATP depletion, and failure of the ATPase ion pumps within the ischemic core. These effects result in accumulation of intracellular sodium and calcium ions. Enhanced calcium influx activates phospholipase A2 (PLA2) to release arachidonic acid (AA) from the membrane, which is converted into 20-hydroxyeicosatetraenoic acid (20-HETE) by CYP4A enzymes. Clotting blood formed after hemorrhagic stroke releases free hemoglobin and serotonin (5-HT). Free hemoglobin scavenges nitric oxide (NO), and the fall in NO level promotes the activity of CYP4A enzymes. 5-HT stimulates PLA2 and releases AA to increase 20-HETE production. The rise of 20-HETE acts on vascular smooth muscle cells leading to vasospasm, further restricting the blood flow to the stroke site and inducing neuron damage. 20-HETE also affects neurons directly by increasing oxidative stress causing expansion of the infarct after ischemic stroke.