Hemodynamic forces in endothelial dysfunction and vascular aging.
Hemodynamic forces in endothelial dysfunction and vascular aging.
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DOI：
10.1016/j.exger.2010.09.010
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发表时间：
2011-02
影响因子：
3.9
通讯作者：
Tzima, Ellie
中科院分区：
文献类型：
--
作者：
Collins, Caitlin;Tzima, Ellie
衰老是与心血管疾病发病相关的关键风险因素。值得注意的是，血管老化和心血管疾病都伴随着内皮功能障碍，或血管扩张剂一氧化氮（NO）的产生和生物利用度的显著降低。由于一氧化氮可用性降低，老化血管通常表现出内皮细胞衰老和氧化应激增加。NO产生的最有效的激活剂之一是由血流产生的流体剪切应力。有趣的是，与年龄相关的NO产生减少部分是由于内皮对剪切应力不敏感。虽然近年来内皮细胞对流体剪切应力的反应已得到很好的表征，但流体剪切应力的机械力如何转化为细胞内生化信号的确切机制相对未知。因此，更好地了解内皮细胞中的机械信号事件可能有助于开发心血管疾病的潜在治疗方法。
Aging is a key risk factor associated with the associated onset of cardiovascular disease. Notably, vascular aging and cardiovascular disease are both with endothelial dysfunction, or a marked decrease in production and bioavailability the vasodilator of nitric oxide (NO). As a result of decreased nitric oxide availability, aging vessels often exhibit endothelial cell senescence and increased oxidative stress. One of the most potent activators of NO production is fluid shear stress produced by blood flow. Interestingly, age-related decrease in NO production partially results from endothelial insensitivity to shear stress. While the endothelial cell response to fluid shear stress has been well characterized in recent years, the exact mechanisms of how the mechanical force of fluid shear stress is converted into intracellular biochemical signals are relatively unknown. Therefore, gaining a better knowledge of mechanosignaling events in endothelial cells may prove to be beneficial for developing potential therapies for cardiovascular diseases.
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DOI：
10.1006/bbrc.1993.1108
发表时间：
1993-02-15
影响因子：
3.1
作者：
ANDO, J;OHTSUKA, A;KAMIYA, A
通讯作者：
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影响因子：
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影响因子：
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作者：
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