Control of cell proliferation in atherosclerosis: insights from animal models and human studies

被引：83

作者：

Fuster, Jose J. ^{[1
]}

Fernandez, Patricia ^{[1
]}

Gonzalez-Navarro, Herminia ^{[1
]}

Silvestre, Carlos ^{[1
,2
]}

Naim Abu Nabah, Yafa ^{[1
]}

Andres, Vicente ^{[1
,2
]}

机构：

[1] Inst Biomed Valencia CSIC, Dept Mol & Cellular Pathol & Therapy, Lab Vasc Biol, Valencia 46010, Spain

[2] Spanish Natl Cardiovasc Res Ctr CNIC, Lab Mol & Genet Cardiovasc Pathophysiol, Dept Atherothrombosis & Cardiovasc Imaging, Madrid 28029, Spain

来源：

CARDIOVASCULAR RESEARCH | 2010年 / 86卷 / 02期

关键词：

Cell cycle; Human atherosclerosis; Animal models atherosclerosis; SMOOTH-MUSCLE-CELLS; SINGLE-NUCLEOTIDE POLYMORPHISM; CORONARY-ARTERY-DISEASE; KINASE INHIBITOR P21; ANTISENSE OLIGONUCLEOTIDES; INTIMAL HYPERPLASIA; CHROMOSOME; 9P21; ENHANCED ATHEROSCLEROSIS; MACROPHAGE PROLIFERATION; DEFICIENCY LEADS;

D O I：

10.1093/cvr/cvp363

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Excessive hyperplastic cell growth within occlusive vascular lesions has been recognized as a key component of the inflammatory response associated with atherosclerosis, restenosis post-angioplasty, and graft atherosclerosis after coronary artery bypass. Understanding the molecular mechanisms that regulate arterial cell proliferation is therefore essential for the development of new tools for the treatment of these diseases. Mammalian cell proliferation is controlled by a large number of proteins that modulate the mitotic cell cycle, including cyclin-dependent kinases, cyclins, and tumour suppressors. The purpose of this review is to summarize current knowledge about the role of these cell cycle regulators in the development of native and graft atherosclerosis that has arisen from animal studies, histological examination of specimens from human patients, and genetic studies.

引用

页码：254 / 264

页数：11

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[31] Antisense oligonucleotide to proto-oncogene c-myb inhibits the formation of intimal hyperplasia in experimental vein grafts [J].