Document Detail


Mechanisms of neointima formation--lessons from experimental models.
MedLine Citation:
PMID:  9546967     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The lamina intima of an artery is the region between the endothelial cell surface and the internal elastic lamina, which forms the luminal margin of the media. In humans the intima of atherosclerosis-prone arteries becomes thicker due to accumulation of smooth muscle cells, which originate from the media. The introduction of percutaneous transluminal coronary angioplasty (PTCA) boosted scientific interest in intimal thickening, because restenosis remains an unresolved problem of this intervention. In order to unravel the mechanisms of intimal thickening there is a need for appropriate animal models. A brief overview of these models is given together with factors that control proliferation and/or migration. Despite intensive research on neointima formation, an effective therapy for restenosis has not emerged to date. This may be due to the fact that other processes, such as acute elastic recoil and chronic constrictive remodeling may contribute to lumen narrowing as well. Other limitations of neointima models are related to species and anatomical differences. Most studies are performed in arteries that are either lesion-free, or contain relatively mild plaques, in contrast to the complicated, stenotic lesions that are the substrate for human PTCA. Other differences are the severity of the injury and incorporation of a mural fibrin-rich thrombus. Nevertheless, studies based on superficial injury, like the frequently used balloon denudation model, are useful. There are similarities with angioplasty, such as endothelial cell damage and proliferation of medial and intimal smooth muscle cells. The use of techniques such as differential display, gene transfer and application of antisense oligonucleotides may provide new therapeutic approaches to reduce neointima formation.
Authors:
G R De Meyer; H Bult
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Vascular medicine (London, England)     Volume:  2     ISSN:  1358-863X     ISO Abbreviation:  Vasc Med     Publication Date:  1997  
Date Detail:
Created Date:  1998-04-13     Completed Date:  1998-04-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9610930     Medline TA:  Vasc Med     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  179-89     Citation Subset:  IM    
Affiliation:
Division of Pharmacology, University of Antwerp-UIA, Wilrijk, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Angioplasty, Transluminal, Percutaneous Coronary
Animals
Arteriosclerosis / pathology*,  physiopathology*
Coronary Thrombosis / pathology,  physiopathology,  therapy
Coronary Vessels*
Disease Models, Animal
Humans
Muscle, Smooth, Vascular / pathology
Tunica Intima / pathology*,  physiopathology*

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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