Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia.

Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Research Abstract Details 

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Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Abstract Text:

Taku Kokubo,Hisashi Uchida,Eric T Choi,

Although major advances have been made in the prevention and treatment of restenosis following coronary and peripheral interventions, the persistent complications of thrombosis and reintervention remain a mainstay for repeat hospitalizations in this patient population. For many years, a ubiquitous cell surface receptor called alpha(v)beta(3) integrin was the target of investigators in the prevention of restenosis because its interaction with the extracellular matrix was believed to coordinate the migration of smooth muscle cells (SMCs) from the media to the intima, the seminal event in the formation of intimal occlusive lesion. After the publication of uniformly positive animal studies demonstrating that alpha(v)beta(3) integrin blockade led to a significant reduction in new intimal (neointimal) lesion formation, early clinical trials supported the association of avoidance of target lesion revascularization and the use of antagonists to the SMC integrin alpha(v)beta(3) and its related platelet integrin alpha(IIb)beta(3). However, a series of clinical trials subsequently demonstrated that these antagonists did not necessarily prevent revascularizations by inhibiting intimal hyperplasia per se. Additional animal studies subsequently showed that, indeed, in the setting of pre-existing SMCs in the intimal lesion (ie, atherosclerotic plaque, fatty streaks), inhibiting SMC migration by way of beta(3) integrin blockade was an ineffective approach in the prevention of intimal hyperplasia and restenosis. However, given the wealth of basic and clinical information on the alpha(v)beta(3) integrin and its antagonists, we discuss in this article our new approach to this old solution by targeting a new clinical problem of early failure arteriovenous access for hemodialysis. Given the uniqueness of arteriovenous access in that there are essentially no significant atherosclerotic lesions in the artery and vein prior to the anastomosis, the seminal event of the migration of SMCs from the media to the neointima could by targeted once again with beta(3) integrin antagonists.

Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Publishing Authors By Initials

T Kokubo,H Uchida,ET Choi,

For similar surgical procedures, operative: cardiovascular surgical procedures: vascular surgical procedures research abstracts see: surgical procedures, operative: cardiovascular surgical procedures: vascular surgical procedures research

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Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Journal Published:

PUBLICATION TYPE: Review

Journal: Journal of vascular surgery : official publication

VOLUME: 45 Suppl A

Page Numbers: A33-8

Journal Abbreviation: J. Vasc. Surg.

ISSN: 0741-5214

DAY: 3

MONTH: Jun

YEAR: 2007

Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8407742

Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Keywords Mesh Terms:

KEYWORDS: Vascular Surgical Procedures

MESH TERMS: adverse effects

Chemical & Substance for Abstract: Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia. Information

Substance Name: Integrin alphaVbeta3

Registry Number: 0

Grant and Affiliation Information for Integrin alpha(v)beta(3) as a target in the prevention of neointimal hyperplasia.

AFFILIATION: Department of Surgery, Washington University School of Medicine, St. Louis, MO, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: K08 HL068119-01A1

ACRONYM: HL

MEDLINETA: J Vasc Surg

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