Mechanical stretch: physiological and pathological implications for human vascular endothelial cells.
Mechanical stretch: physiological and pathological implications for human vascular endothelial cells.
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DOI：
10.1186/s13221-015-0033-z
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Baker MS
中科院分区：
文献类型：
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作者：
Jufri NF;Mohamedali A;Avolio A;Baker MS
由于血流的脉动性质，血管内皮细胞受到血液动力学力，例如机械拉伸。不同强度的机械拉伸由细胞表面上的机械感受器检测，这使得外部机械刺激能够转化为细胞中的生化信号，激活下游信号传导途径。这种激活可以根据细胞是否暴露于生理或病理拉伸强度而变化。与正常生理功能相关的实质性拉伸在维持血管稳态中是重要的，因为它涉及细胞结构的调节、血管生成、增殖和血管张力的控制。然而，伴随高血压发生的升高的压力使细胞暴露于过度的机械负荷，并且这可能通过形成活性氧、炎症和/或凋亡而导致病理后果。这些过程由下游信号通过决定细胞命运的各种途径激活。参与这些过程的蛋白质的鉴定可能有助于阐明与病理性机械拉伸相关的血管疾病的新机制，并可能为旨在对抗这些机制的负面影响的治疗策略提供新的见解。
Vascular endothelial cells are subjected to hemodynamic forces such as mechanical stretch due to the pulsatile nature of blood flow. Mechanical stretch of different intensities is detected by mechanoreceptors on the cell surface which enables the conversion of external mechanical stimuli to biochemical signals in the cell, activating downstream signaling pathways. This activation may vary depending on whether the cell is exposed to physiological or pathological stretch intensities. Substantial stretch associated with normal physiological functioning is important in maintaining vascular homeostasis as it is involved in the regulation of cell structure, vascular angiogenesis, proliferation and control of vascular tone. However, the elevated pressure that occurs with hypertension exposes cells to excessive mechanical load, and this may lead to pathological consequences through the formation of reactive oxygen species, inflammation and/or apoptosis. These processes are activated by downstream signaling through various pathways that determine the fate of cells. Identification of the proteins involved in these processes may help elucidate novel mechanisms involved in vascular disease associated with pathological mechanical stretch and could provide new insight into therapeutic strategies aimed at countering the mechanisms’ negative effects.