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(Hypertension. 2006;48:1026.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

CuZn Superoxide Dismutase Deficiency

Culprit of Accelerated Vascular Aging Process

Dan-Dan Chen; Alex F. Chen

From the Departments of Pharmacology and Neurology, Neuroscience Program and Cell and Molecular Biology Program, Michigan State University, East Lansing, Mich.

Correspondence to Alex F. Chen, Department of Pharmacology and Toxicology, B403 Life Sciences Building, Michigan State University, East Lansing, MI 48824-1317. E-mail chenal@msu.edu

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

Impairment of endothelium-dependent responses is an early landmark of endothelial dysfunction in blood vessels with aging and/or cardiovascular diseases.¹ A critical manifestation of endothelial dysfunction is the reduced bioavailability of NO, a key vascular protective molecule and an independent predictor of cardiovascular events.² Hence, stimuli decreasing vascular NO bioavailability manifest impaired endothelium-dependent relaxation.

Aging is associated with marked changes in the cardiovascular system, especially at the level of the vascular wall.³ Both structural and functional changes can take place at the level of the endothelium, vascular smooth muscle cell (VSMC), and the extracellular matrix of blood vessels. Endothelial thickening and altered endothelium-dependent responses have been reported in aged animals. Clinical studies have also shown that endothelium-dependent relaxation of both conduit and resistance vessels declines progressively with age. In contrast, endothelium-independent relaxation to sodium nitroprusside is unaffected by aging, suggesting that the impaired relaxation with age is primarily because of the dysfunctional endothelium, rather than VSMC contraction.³

Although the mechanisms underlying the aging-induced endothelial dysfunction are complex and incompletely understood, oxidative stress is a key contributor.⁴ Exposure of endothelial cells to increased levels of reactive oxygen species (ROS) during the aging process makes them a prime target for oxidative stress. As the first and initiating oxygen free radical in the ROS chain, superoxide (O₂^–) consumption of NO is one of the most important mechanisms of endothelial dysfunction.⁵ Vascular cells possess multifaceted protective mechanisms against the toxic effects of ROS.^4–6 Among them, the 3 superoxide dismutase (SOD) isoforms, the cytosolic copper . . . [Full Text of this Article]

Related Article:

Heterozygous CuZn Superoxide Dismutase Deficiency Produces a Vascular Phenotype With Aging

Sean P. Didion, Dale A. Kinzenbaw, Laura I. Schrader, and Frank M. Faraci
Hypertension 2006 48: 1072-1079. [Abstract] [Full Text] [PDF]