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Atherosclerosis
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DOI：10.1016/S0003-4975(97)00961-2.png)
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Abstract
En 中文
Most of the indications for cardiovascular operation and many of its complications are in large part due to advanced atherosclerosis. The pathogenesis of atherosclerosis involves inflammatory infiltration of the vessel wall, cellular proliferation, fibrous plaque formation, and ultimately plaque rupture and occlusive thrombosis. Many of these events are linked, at least initially, to chronic injury of the vascular endothelium. Endothelial cell injury from hypertension, diabetes mellitus, hyperlipidemia, fluctuating shear stress, smoking, or transplant rejection disrupts normal endothelial cell function. This results in the loss of the constitutive protective mechanisms and an increase in inflammatory, procoagulant, vasoactive, and fibroproliferative responses to injury. These changes promote vasospasm, intimal proliferation, and thrombus formation, all of which play a significant role in the initiation, progression, and clinical manifestations of atherosclerosis. Understanding the role of the chronically injured endothelium and its interactions with circulating immune cells and the underlying smooth muscle cells may lead to novel therapeutic interventions for the prevention and treatment of atherosclerosis. (C) 1997 by The Society of Thoracic Surgeons.
Keywords:
HUMAN-ENDOTHELIAL-CELLS
SMOOTH-MUSCLE CELLS
TRANSFORMING GROWTH-FACTOR
CORONARY-ARTERY DISEASE
VASCULAR ENDOTHELIUM
PROCOAGULANT ACTIVITY
CHRONIC REJECTION
GENE-EXPRESSION
FACTOR-ALPHA
INTERLEUKIN-1
Journal
IF:
3.9
Papers:
2.8W
Citations:
3.4W
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Cited Papers
1989 CORCORAN LECTURE - ADAPTIVE AND MALADAPTIVE RESPONSES OF THE ARTERIAL-WALL TO HYPERTENSION.png)
HYPERTENSION
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HYPERTENSIONIF8.2
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