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(Circulation. 2008;117:3060-3061.)
© 2008 American Heart Association, Inc.

Editorial

Origin of Cells That Contribute to Neointima Growth

Hiroshi Iwata, MD, PhD; Masataka Sata, MD, PhD

From the Department of Cardiovascular Medicine (H.I., M.S.), University of Tokyo Graduate School of Medicine, Tokyo, Japan; Department of Cardiovascular Medicine (M.S.), Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan; and Department of Advanced Clinical Science and Therapeutics (M.S.), University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Correspondence to Masataka Sata, MD, PhD, Professor and Chairman, Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan. E-mail sata@clin.med.tokushima-u.ac.jp

Key Words: Editorials • restenosis • angioplasty • lesion • inflammation • leukocytes

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

Percutaneous coronary interventions (PCIs) have become widely adopted for treatment of coronary atherosclerosis. Although there is increasing use of new devices, restenosis still limits the long-term outcome of PCI.¹ Histological studies revealed that uninhibited cell accumulation in the neointima plays a principal role in the pathogenesis of post-PCI restenosis.¹ Many studies have documented that the majority of neointimal cells express some markers of smooth muscle cells (SMCs).¹ Thus, it was generally believed that SMCs in the adjacent medial layer migrate into the subendothelial space, proliferate, and synthesize extracellular matrix, thereby contributing to neointima formation.² It was hypothesized that all neointimal SMCs in post-PCI restenosis are derived from medial SMCs.²

Article p 3079

On the other hand, it has been noted that neointimal SMCs are quite distinct from medial SMCs. The SMCs of the normal adult vessel wall display characteristics of a differentiated and contractile phenotype. In contrast, neointimal cells are characterized by a large cell body that contains synthetic and secretary organelles. These "synthetic" SMCs secrete extracellular matrix components and express lower levels of the smooth muscle–specific contractile proteins.³ Although "contractile" SMCs are quiescent in the cell cycle, synthetic SMCs proliferate and migrate in response to various growth factors.⁴ To explain the origin of synthetic SMCs observed in restenotic lesions, it has been proposed that contractile SMCs of the media dedifferentiate into synthetic SMCs in response to various cytokines secreted by the infiltrating inflammatory cells.² Therefore, much effort has been devoted to understanding the regulators of the vascular SMC phenotype . . . [Full Text of this Article]