Endothelial Targets in Stroke

Author:

Andjelkovic Anuska V.12,Xiang Jianming1,Stamatovic Svetlana M.2,Hua Ya1,Xi Guohua1,Wang Michael M.34,Keep Richard F.14

Affiliation:

1. From the Departments of Neurosurgery (A.V.A., J.X., Y.H., G.X., R.F.K.), University of Michigan, Ann Arbor and Department of Veterans Affairs, Neurology Service, VA Ann Arbor Healthcare System, MI.

2. Pathology (A.V.A., S.M.S.), University of Michigan, Ann Arbor and Department of Veterans Affairs, Neurology Service, VA Ann Arbor Healthcare System, MI.

3. Neurology (M.M.W.), University of Michigan, Ann Arbor and Department of Veterans Affairs, Neurology Service, VA Ann Arbor Healthcare System, MI.

4. Molecular and Integrative Physiology (M.M.W., R.F.K.), University of Michigan, Ann Arbor and Department of Veterans Affairs, Neurology Service, VA Ann Arbor Healthcare System, MI.

Abstract

Cerebral ischemia (stroke) induces injury to the cerebral endothelium that may contribute to parenchymal injury and worsen outcome. This review focuses on current preclinical studies examining how to prevent ischemia-induced endothelial dysfunction. It particularly focuses on targets at the endothelium itself. Those include endothelial tight junctions, transcytosis, endothelial cell death, and adhesion molecule expression. It also examines how such studies are being translated to the clinic, especially as adjunct therapies for preventing intracerebral hemorrhage during reperfusion of the ischemic brain. Identification of endothelial targets may prove valuable in a search for combination therapies that would specifically protect different cell types in ischemia.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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