The role of cellular adaptation to mechanical forces in atherosclerosis.
The role of cellular adaptation to mechanical forces in atherosclerosis.
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DOI：
10.1161/atvbaha.108.165951
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发表时间：
2008-12
期刊：
影响因子：
--
通讯作者：
Schwartz MA
中科院分区：
文献类型：
--
作者：
Hahn C;Schwartz MA
动脉粥样硬化是一种慢性炎症性疾病，起源于暴露于流体流动干扰的动脉区域，并导致这些区域中进行性斑块形成。最近关于细胞对流动的反应的工作已经确定了可能影响疾病进展的潜在机械传感器和途径。这些结果使我们假设，同样的机制，调解适应性反应的血管系统成为适应不良的网站的干扰流。基因表达和基质重塑的后续变化有助于夹带这些炎症通路。这些事件与高脂血症、吸烟和糖尿病等全身性风险因素协同作用，导致疾病进展。
Atherosclerosis is a chronic inflammatory disease that originates at regions of arteries exposed to disturbances in fluid flow and results in progressive plaque formation in those areas. Recent work on cellular responses to flow has identified potential mechanosensors and pathways that may influence disease progression. These results lead us to hypothesize that the same mechanisms that mediate adaptive responses in the vasculature become maladaptive at sites of disturbed flow. Subsequent changes in gene expression and matrix remodeling help to entrain these inflammatory pathways. These events synergize with systemic risk factors such as hyperlipidemia, smoking and diabetes, leading to disease progression.