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机械牵张:对人血管内皮细胞的生理和病理影响

Mechanical stretch: physiological and pathological implications for human vascular endothelial cells.

作者信息

Jufri Nurul F, Mohamedali Abidali, Avolio Alberto, Baker Mark S

机构信息

Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, F10A, 2 Technology Place, Macquarie University, Sydney, NSW 2109 Australia.

Department of Chemistry & Biomolecular Sciences, F7B Building Research Park Drive, Macquarie University, Sydney, NSW 2109 Australia.

出版信息

Vasc Cell. 2015 Sep 18;7:8. doi: 10.1186/s13221-015-0033-z. eCollection 2015.

DOI:10.1186/s13221-015-0033-z
PMID:26388991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4575492/
Abstract

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.

摘要

由于血流的脉动特性,血管内皮细胞受到诸如机械拉伸等血流动力学力的作用。细胞表面的机械感受器可检测到不同强度的机械拉伸,这使得外部机械刺激能够转化为细胞内的生化信号,从而激活下游信号通路。这种激活可能因细胞暴露于生理或病理拉伸强度而有所不同。与正常生理功能相关的显著拉伸对于维持血管稳态很重要,因为它参与细胞结构的调节、血管生成、增殖以及血管张力的控制。然而,高血压时出现的血压升高会使细胞暴露于过度的机械负荷下,这可能通过活性氧的形成、炎症和/或细胞凋亡导致病理后果。这些过程通过各种途径的下游信号传导被激活来决定细胞的命运。鉴定参与这些过程的蛋白质可能有助于阐明与病理机械拉伸相关的血管疾病的新机制,并可为旨在对抗这些机制负面影响的治疗策略提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/0429451abc0c/13221_2015_33_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/b27c73cb572d/13221_2015_33_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/3b6c80303682/13221_2015_33_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/0429451abc0c/13221_2015_33_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/b27c73cb572d/13221_2015_33_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/3b6c80303682/13221_2015_33_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cf9/4575492/0429451abc0c/13221_2015_33_Fig3_HTML.jpg

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