NR4A Nuclear Receptors in Atherosclerosis and Vein-Graft Disease

Nur77, Nurr1, and NOR-1 form the NR4A subfamily of the nuclear hormone receptor superfamily of transcription factors and have been described in the regulation of differentiation, proliferation, apoptosis, and survival of many different cell types. The expression of NR4A nuclear receptors in vascular...

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Bibliographic Details
Published in:Trends in cardiovascular medicine 2007-04, Vol.17 (3), p.105-111
Main Authors: Bonta, Peter I, Pols, Thijs W.H, de Vries, Carlie J.M
Format: Article
Language:English
Subjects:
Angina pectoris
Animals
Apoptosis
Atherosclerosis
Atherosclerosis - metabolism
Atherosclerosis - pathology
Cardiovascular
Cell cycle
Cell Differentiation
Cell Proliferation
Cell Survival
Cytokines
Disease
DNA-Binding Proteins - metabolism
Genotype & phenotype
Graft Occlusion, Vascular - metabolism
Graft Occlusion, Vascular - pathology
Heart attacks
Humans
Kinases
Ligands
Membrane Transport Proteins - metabolism
Muscle, Smooth, Vascular - blood supply
Muscle, Smooth, Vascular - cytology
Myocytes, Smooth Muscle - metabolism
Nerve Tissue Proteins - metabolism
Nuclear Receptor Subfamily 4, Group A, Member 1
Nuclear Receptor Subfamily 4, Group A, Member 2
Proteins
Receptors, Cell Surface - metabolism
Receptors, Cytoplasmic and Nuclear - metabolism
Receptors, Steroid - metabolism
Recruitment
Transcription Factors - metabolism
Veins & arteries
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Summary:Nur77, Nurr1, and NOR-1 form the NR4A subfamily of the nuclear hormone receptor superfamily of transcription factors and have been described in the regulation of differentiation, proliferation, apoptosis, and survival of many different cell types. The expression of NR4A nuclear receptors in vascular pathologies has only recently been revealed, after which studies on the functional involvement of NR4A receptors in vascular disease were initiated. This review summarizes our current view on involvement of Nur77, Nurr1, and NOR-1 in atherosclerotic vascular disease and discusses NR4A function in vascular response to injury.
ISSN:1050-1738
1873-2615
DOI:10.1016/j.tcm.2007.02.001