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(Circulation Research. 2005;97:1083.)
© 2005 American Heart Association, Inc.

Editorials

The Translation of Transcription

Sorin Pislaru, Robert D. Simari

From the Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn.

Correspondence to Robert D. Simari, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. E-mail simari.robert@mayo.edu

See related article, pages 1132–1141

Key Words: transcription factors • restenosis • vascular smooth muscle

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

Defining the factors that mediate the phenotype of vascular smooth muscle cells (VSMCs) is important in the identification of new therapeutic targets for vascular diseases that are associated with VSMC phenotypic modulation. This modulation is characterized by a switch from a quiescent "contractile" state to an activated "synthetic" state and is an integral part of the acute response to vascular injury.¹ This phenotypic switch is the result of a complex pattern of gene regulation suggesting an important role for regulation at a transcriptional level. As such, transcription factors involved in this regulation may be "druggable" targets for the prevention and treatment of vascular diseases. In this issue of Circulation Research, an article by Fujiu and colleagues² adds an important new chapter in a translational story that began with the identification of Kruppel-like zinc-finger transcription factor 5 (KLF5) and its role in transcriptional regulation of VSMCs. KLF5 is a key determinant of smooth muscle phenotype³ through regulation of expression of a number of proteins associated with a quiescent or contractile phenotype including SMemb/non-myosin heavy chain-B (NMMHC-B), platelet-derived growth factor-A (PDGF-A), and smooth muscle -actin. This new study demonstrates that inhibition of this transcription factor may represent an exciting new modality to prevent or treat the vascular response to injury associated with phenotypic modulation of VSMCs including restenosis.

Soon after Andreas Gruentzig presented the first human experience with percutaneous coronary angioplasty, it was recognized that the initial success of coronary interventions is lost in a significant number of patients because of . . . [Full Text of this Article]

Related Article:

Synthetic Retinoid Am80 Suppresses Smooth Muscle Phenotypic Modulation and In-Stent Neointima Formation by Inhibiting KLF5

Katsuhito Fujiu, Ichiro Manabe, Atsushi Ishihara, Yumiko Oishi, Hiroshi Iwata, Go Nishimura, Takayuki Shindo, Koji Maemura, Hiroyuki Kagechika, Koichi Shudo, and Ryozo Nagai
Circ. Res. 2005 97: 1132-1141. [Abstract] [Full Text] [PDF]