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(Circulation Research. 2007;101:331.)
© 2007 American Heart Association, Inc.

Editorials

ecSOD Controls the Delicate Balance of Reactive Oxygen Species in Bone Marrow and Ischemic Tissue Needed for Neovascularization

Michael S. Wolin

From the Departments of Physiology, New York Medical College, Valhalla, NY.

Correspondence to Michael S. Wolin, PhD, Department of Physiology, Basic Science Building, Rm. 604, New York Medical College, Valhalla, NY 10595. E-mail mike_wolin@nymc.edu

See related articles, pages 409–419

Key Words: endothelium • nitric oxide • ischemic biology • oxidant stress

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

"In this issue of Circulation Research, Tohru Fukai and colleagues (1) provide evidence from a mouse hindlimb ischemia model indicating that the superoxide anion scavenging activity of the secreted extracellular form of superoxide dismutase (ecSOD) has an apparently essential role in enabling neovascularization to occur." Both reactive oxygen species (ROS) and nitric oxide (NO) appear to be part of many of the signaling mechanisms in individual cell types and subcellular environments influencing key processes (shown in the Figure) that both enable and prevent the restoration of impaired blood flow to ischemic tissue through neovascularization. Thus, it seems rather remarkable that the ecSOD system has such an important role in controlling the balance of processes involved. Moreover, ecSOD appears to be a key regulator of the mobilization of circulating inflammatory and endothelial progenitor cells (EPCs) from bone marrow, which are major contributors to inflammation driven vascular growth promoting processes involved in neovascularization.

View larger version (13K):   Model showing the potential role of an increase in ecSOD caused by hindlimb ischemia in modulating ROS and NO-derived species and processes potentially regulated by changes in the balance of redox signaling that potentially contribute to the reparative neovascularization based on studies in mice deficient in ecSOD.

Hindlimb ischemia is shown in the Fukai study to increase the expression of ecSOD both in the ischemic muscle tissue and in bone marrow. The importance of this observation is highlighted by data showing that exposure of mice deficient in ecSOD to hindlimb ischemia was associated with decreased NO-cGMP signaling . . . [Full Text of this Article]

Related Article:

Essential Role of Extracellular SOD in Reparative Neovascularization Induced by Hindlimb Ischemia

Ha Won Kim, Angela Lin, Robert E. Guldberg, Masuko Ushio-Fukai, and Tohru Fukai
Circ. Res. 2007 101: 409-419. [Abstract] [Full Text] [PDF]