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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:715.)
© 2002 American Heart Association, Inc.

Editorials

PTEN-uating Restenosis

Stefanie Dimmeler; Andreas M. Zeiher

From the Division of Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Germany.

Correspondence to Stefanie Dimmeler PhD, Division of Molecular Cardiology, Dept. of Internal Medicine IV, University of Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany. E-mail Dimmeler@em.uni-frankfurt.de

Within the last few years, the lipid phosphatase PTEN has gained increasing attention.¹ Initially described as a tumor suppressor gene, the function of PTEN meanwhile ranges from the regulation of the immune system to the recently established important function in neuronal growth.^1,2 On a cellular level, PTEN interferes with cell proliferation, survival, and growth. These effects are not restricted to a certain cell type or species but have been demonstrated from Drosophila to humans and in various cell types including cardiomyocytes.^2–4 Consistent with a crucial role for PTEN in the regulation of cell fate, the complete deficiency of PTEN leads to embryonic lethality in mice.^5,6 On a molecular level, PTEN dephosphorylates phosphatidylinositol-(3,4,5) trisphosphate [PtdIns (3,4,5)P₃], which is formed by the phosphatidylinositol-3-kinase (PI3K).⁴ Thereby, PTEN antagonizes the diverse downstream signaling effector pathways activated by PI3K-derived phospholipids (Figure).

View larger version (40K): [in this window] [in a new window]   Schematic illustration of the molecular signaling pathways influenced by PTEN: potential role in regulation of smooth muscle cell proliferation, survival, and apoptosis. PTEN dephosphorylates the PtdIns(3,4,5)P3 and thereby prevents activation of downstream effector pathways including the phosphoinositide-dependent kinases (PDK).

See page 745

Now, in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, the article of Huang and Kontos⁷ adds a new twist to the multifactorial roles of PTEN. The results of this study suggest that PTEN may comprise a new bullet against restenosis. Restenosis is the most important limitation of balloon angioplasty or stent placement and occurs in 20% to 40% of patients within the first few months after successful . . . [Full Text of this Article]