Document Detail


Cellular, molecular and immunological mechanisms in the pathophysiology of vein graft intimal hyperplasia.
MedLine Citation:
PMID:  16519729     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Coronary artery disease, leading to myocardial infarction and ischaemia, affects millions of persons and is one of the leading causes of morbidity and mortality worldwide. Invasive techniques such as coronary artery bypass grafting are used to alleviate the sequelae of arterial occlusion. Unfortunately, restenosis or occlusion of the grafted conduit occurs over a time frame of months to years with a gradual reduction in patency, especially in vein grafts. The events leading to intimal hyperplasia (IH) formation involve numerous cellular and molecular components. Various cellular elements of the vessel wall are involved as are leucocyte-endothelial interactions that trigger the coagulation cascade leading to localized thrombus formation. Subsequent phenotypic modification of the medial smooth muscle cells and their intimal migration is the basis of the lesion formation that is thought to be propagated by an immune-mediated reaction. Despite intense scrutiny, the pathophysiology of IH remains an enigma. Although several growth factors, cytokines and numerous other biomolecules have been implicated and their relationship to prohyperplasia pathways such as the phosphatidyl-inositol 3-kinase (PI3K)-Akt pathway has been established, many pieces of the puzzle are still missing. An in-depth understanding of early vein graft adaptation and progression is necessary to improve the long-term prognosis and develop more effective therapeutic measures. In this review, we have critically evaluated and summarized the literature to elucidate and interlink the numerous established and emerging factors that play a key role in the development of IH leading to vein graft restenosis.
Authors:
Amit K Mitra; Deepak M Gangahar; Devendra K Agrawal
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Immunology and cell biology     Volume:  84     ISSN:  0818-9641     ISO Abbreviation:  Immunol. Cell Biol.     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-03-07     Completed Date:  2006-07-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8706300     Medline TA:  Immunol Cell Biol     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  115-24     Citation Subset:  IM    
Affiliation:
Department of Biomedical Sciences, Creighton University School of Medicine, Omaha, NE 68178, USA.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / immunology
Arterial Occlusive Diseases / etiology,  immunology,  mortality,  pathology
Coronary Artery Bypass* / adverse effects,  mortality
Graft Occlusion, Vascular / etiology,  immunology*,  pathology
Graft Survival / immunology*
Growth Substances / immunology
Humans
Hyperplasia / etiology,  immunology,  mortality,  pathology
Immunity, Cellular
Leukocytes / immunology*,  pathology
Myocardial Infarction / complications,  immunology,  mortality,  surgery
Oncogene Protein v-akt / immunology
Signal Transduction / immunology*
Tunica Intima / immunology*,  pathology
Grant Support
ID/Acronym/Agency:
R01HL070885/HL/NHLBI NIH HHS; R01HL07349/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Growth Substances; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Oncogene Protein v-akt

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


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