Mechanical stretch: Physiological and pathological implications for human vascular endothelial cells

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

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

97 Citations (Scopus)
63 Downloads (Pure)

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.

Original languageEnglish
Article number8
Pages (from-to)1-12
Number of pages12
JournalVascular Cell
Volume7
Issue number1
DOIs
Publication statusPublished - 18 Sep 2015

Bibliographical note

Copyright the Author(s) 2015. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

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