Control of cell proliferation in atherosclerosis: insights from animal models and human studies.
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.
Fuster
José J
JJ
Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia-CSIC, C/Jaime Roig 11, 46010 Valencia, Spain.
Fernández
Patricia
P
González-Navarro
Herminia
H
Silvestre
Carlos
C
Nabah
Yafa Naim Abu
YN
Andrés
Vicente
V
D000818:Animals; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D001808:Blood Vessels / Q000378:metabolism / Q000473:pathology*; D002453:Cell Cycle / Q000235:genetics; D018797:Cell Cycle Proteins / Q000378:metabolism; D049109:Cell Proliferation; D004195:Disease Models, Animal; D006801:Humans; D006965:Hyperplasia; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
D018797:Cell Cycle Proteins