Autophagy and mechanotransduction in outflow pathway cells.

Journal Article (Journal Article;Review)

Because of elevations in IOP and other forces, cells in the trabecular meshwork (TM) are constantly subjected to mechanical strain. In order to preserve cellular function and regain homeostasis, cells must sense and adapt to these morphological changes. We and others have already shown that mechanical stress can trigger a broad range of responses in TM cells; however, very little is known about the strategies that TM cells use to respond to this stress, so they can adapt and survive. Autophagy, a lysosomal degradation pathway, has emerged as an important cellular homeostatic mechanism promoting cell survival and adaptation to a number of cytotoxic stresses. Our laboratory has reported the activation of autophagy in TM cells in response to static biaxial strain and high pressure. Moreover, our newest data also suggest the activation of chaperon-assisted selective autophagy, a recently identified tension-induced autophagy essential for mechanotransduction, in TM cells under cyclic mechanical stress. In this review manuscript we will discuss autophagy as part of an integrated response triggered in TM cells in response to strain, exerting a dual role in repair and mechanotransduction, and the potential effects of dysregulated in outflow pathway pathophysiology.

Full Text

Duke Authors

Cited Authors

  • Hirt, J; Liton, PB

Published Date

  • May 2017

Published In

Volume / Issue

  • 158 /

Start / End Page

  • 146 - 153

PubMed ID

  • 27373974

Pubmed Central ID

  • PMC5199638

Electronic International Standard Serial Number (EISSN)

  • 1096-0007

Digital Object Identifier (DOI)

  • 10.1016/j.exer.2016.06.021


  • eng

Conference Location

  • England