Intimal hyperplasia: slow but deadly
Autor: | B Mills, T Robb, Douglas F. Larson |
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Rok vydání: | 2012 |
Předmět: |
medicine.medical_specialty
Pathology Vascular smooth muscle Intimal hyperplasia medicine.medical_treatment Cell Growth Processes Muscle Smooth Vascular Internal medicine Angioplasty medicine Humans Radiology Nuclear Medicine and imaging Vascular Diseases PI3K/AKT/mTOR pathway Advanced and Specialized Nursing Hyperplasia business.industry General Medicine medicine.disease Internal elastic lamina Endothelial stem cell medicine.anatomical_structure Cardiology Tunica Intima Cardiology and Cardiovascular Medicine business Safety Research Artery |
Zdroj: | Perfusion. 27:520-528 |
ISSN: | 1477-111X 0267-6591 |
DOI: | 10.1177/0267659112452316 |
Popis: | Intimal hyperplasia is the leading cause of long-term failure in coronary artery bypass vein grafting, coronary artery stenting, angioplasty, arteriovenous fistula for dialysis, and allograft transplantation. Intimal hyperplasia is a product of vascular smooth muscle cell proliferation, migration through the internal elastic lamina, and deposition of extracellular matrix proteins driven by growth factors in the vasculature. This vascular pathology results in a progressive diminution of the vessel lumen and serves as a site for thrombosis and atherosclerotic lesions. A key cell type in the initiation of intimal hyperplasia is the vascular endothelial cell, which appears to have down-stream effects on the vascular smooth muscle proliferation and migration. Currently, the only means available for prevention of intimal hyperplasia is through inhibition of mammalian target of rapamycin (mTOR) with the immunosuppressant rapamycin. mTOR integrates up-stream signals from growth factors such as IL-2 and senses the cellular nutrient and energy levels and redox status. This presentation will discuss the potential means of preserving the vascular endothelial cell and, thereby, reducing the development of intimal hyperplasia in our open-heart surgical patients. |
Databáze: | OpenAIRE |
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