新生内膜
细胞外基质
血管平滑肌
胚胎血管重塑
内皮
肌肉肥大
血管
医学
细胞生物学
病理
内科学
解剖
心脏病学
生物
再狭窄
支架
平滑肌
作者
Muhammad Anwar,Joseph Shalhoub,C.W. Lim,Manjit S. Gohel,Alexander Giles Davies
出处
期刊:Journal of Vascular Research
[S. Karger AG]
日期:2012-01-01
卷期号:49 (6): 463-478
被引量:173
摘要
High blood pressure is responsible for the modulation of blood vessel morphology and function. Arterial hypertension is considered to play a significant role in atherosclerotic ischaemic heart disease, stroke and hypertensive nephropathy, whereas high venous pressure causes varicose vein formation and chronic venous insufficiency and contributes to vein bypass graft failure. Hypertension exerts differing injurious forces on the vessel wall, namely shear stress and circumferential stretch. Morphological and molecular changes in blood vessels ascribed to elevated pressure consist of endothelial damage, neointima formation, activation of inflammatory cascades, hypertrophy, migration and phenotypic changes in vascular smooth muscle cells, as well as extracellular matrix imbalances. Differential expression of genes encoding relevant factors including vascular endothelial growth factor, endothelin-1, interleukin-6, vascular cell adhesion molecule, intercellular adhesion molecule, matrix metalloproteinase-2 and -9 and plasminogen activator inhibitor-1 has been explored using ex vivo cellular or organ stretch models and in vivo experimental animal models. Identification of pertinent genes may unravel new therapeutic strategies to counter the effects of pressure-induced stretch on the vessel wall and hence minimise its notable complications.
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