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Stroke. 2003;34:327-329
doi: 10.1161/01.STR.0000054052.52510.2C
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(Stroke. 2003;34:327.)
© 2003 American Heart Association, Inc.


Advances in Stroke 2002

Vascular Protection

Frank M. Faraci, PhD

From the Departments of Internal Medicine and Pharmacology, Cardiovascular Center, University of Iowa Carver College of Medicine, Iowa City.

Correspondence to Frank M. Faraci, PhD, Department of Internal Medicine, E315-GH, University of Iowa, Carver College of Medicine, Iowa City, IA 52242-1081. E-mail frank-faraci@uiowa.edu


Key Words: endothelium • nitric oxide • oxygen radical • superoxide dismutase


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

In contrast to the emphasis that has been placed on studies of neuroprotection, relatively few studies have addressed mechanisms of vascular protection in the cerebral circulation. Studies in this area have broad potential, because advances in our understanding of molecular mechanisms that contribute to and protect from vascular dysfunction could eventually lead to development of more effective therapies for cardiovascular disease. This editorial will highlight some recent advances related to vascular protection in brain.

Superoxide Dismutases

At relatively low concentrations, superoxide and other reactive oxygen species play important roles, including acting as mediators in signaling processes and regulation of gene expression. High levels of reactive oxygen species contribute to abnormal cell growth and vascular dysfunction. For example, there is recent evidence for increased superoxide in cerebral circulation after subarachnoid hemorrhage (SAH), in the presence of hyperhomocystinemia and diabetes, and in response to angiotensin II or alcohol.1–5

Local steady-state levels of superoxide are dependent on both the rate of superoxide production and activity of endogenous superoxide dismutases (SODs) (Figure). There are 3 isoforms of SOD (cytosolic or CuZn-SOD [SOD-1], mitochondrial or Mn-SOD [SOD-2], and extracellular CuZn-SOD [EC-SOD, SOD-3]), which are localized in distinct subcellular compartments (Figure). Although recent studies in nonvascular cells suggest that these different isoforms have major but distinctive roles,6 the functional importance of individual SOD isoforms has been unclear for any blood vessel.


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Schematic illustration of how superoxide (O2-) is dismuted by the 3 superoxide dismutases (CuZn-SOD, Mn-SOD, and EC-SOD) to H2O2. NO . . . [Full Text of this Article]




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