Molecular mechanisms in intimal hyperplasia.
Intimal hyperplasia is the process by which the cell population increases within the innermost layer of the arterial wall, such as occurs physiologically during closure of the ductus arteriosus and during involution of the uterus. It also occurs pathologically in pulmonary hypertension, atherosclerosis, after angioplasty, in transplanted organs, and in vein grafts. The underlying causes of intimal hyperplasia are migration and proliferation of vascular smooth muscle cells provoked by injury, inflammation, and stretch. This review discusses, at a molecular level, both the final common pathways leading to smooth muscle migration and proliferation and their (patho)-physiological triggers. It emphasizes the key roles played by growth factors and extracellular matrix-degrading metalloproteinases, which act in concert to remodel the extracellular matrix and permit cell migration and proliferation.
Newby
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Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol BS2 8HW, UK. A.Newsby@bris.ac.uk
Zaltsman
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AB
D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000502:physiology*; D016228:Endothelial Growth Factors / Q000502:physiology; D006801:Humans; D006965:Hyperplasia / Q000209:etiology / Q000473:pathology; D008666:Metalloendopeptidases / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D017539:Tunica Intima / Q000473:pathology*
D016228:Endothelial Growth Factors; D008666:Metalloendopeptidases