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Cardiovascular Research 2004 61(2):204-205; doi:10.1016/j.cardiores.2003.12.002
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

LDL, IGF-1, and VSMC apoptosis: linking atherogenesis to plaque rupture in vulnerable lesions

Edward F LaBellea,* and Thomas N Tulenkob

aDepartment of Pathobiology, University of Pennsylvania School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce St., Philadelphia, PA 19104, USA
bDepartments of Surgery, Biochemistry, and Molecular Pharmacology, Thomas Jefferson University School of Medicine, 1025 Walnut Street, Suite 605, Philadelphia, PA 19107, USA

* Corresponding author. Tel.: +1-215-8988856; fax: +1-215-7622299. labelle@vet.upenn.edu

Received 26 November 2003; accepted 2 December 2003

KEYWORDS LDL; IGF-1; Vascular smooth muscle; Apoptosis; Atherosclerosis

The first 10% of the full text of this article appears below.

See article by Gonzales-Timon [12] (pages 247–255) in this issue.

Vascular smooth muscle cells (VSMC) play an important role in the sequence of events leading to the formation of atherosclerotic lesions. VSMC that normally reside in the arterial media undergo a series of phenotypic changes and migrate to the arterial intima where they proliferate and secrete extracellular matrix that contributes to the formation of the protective fibrous cap. Eventually these "synthetic" VSMC [1] can undergo . . . [Full Text of this Article]


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