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Exp Eye Res. 2017 Apr;157:13-19. doi: 10.1016/j.exer.2017.02.005. Epub 2017 Feb 20.

Biomechanical aspects of axonal damage in glaucoma: A brief review.

Author information

1
Optic Nerve Head Research Laboratory, Discoveries in Sight Research Laboratories, Devers Eye Institute, Legacy Health System, Portland, Oregon, USA.
2
Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany.
3
Department of Biomedical Engineering, Georgia Institute of Technology/Emory University, Atlanta, GA, USA. Electronic address: ross.ethier@bme.gatech.edu.
4
Harvard University, Cambridge, MA, USA.
5
University of Alabama, Birmingham, AL, USA.
6
University of California, San Diego, CA, USA.
7
University of California, Santa Barbara, CA, USA.
8
Devers Eye Institute, Portland, OR, USA.
9
University College London, London, UK.
10
Harvard Medical School, Boston, MA, USA.
11
University of Pennsylvania, Philadelphia, PA, USA.
12
Oregon Health and Science University, Portland, OR, USA.
13
New York Medical College, Valhalla, NY, USA.
14
University of Pittsburgh, Pittsburgh, PA, USA.
15
University of California, Los Angeles, CA, USA.
16
Massachusetts Eye and Ear, Boston, MA, USA.
17
Baylor College of Medicine, Houston, TX, USA.

Abstract

The biomechanical environment within the optic nerve head (ONH) is complex and is likely directly involved in the loss of retinal ganglion cells (RGCs) in glaucoma. Unfortunately, our understanding of this process is poor. Here we describe factors that influence ONH biomechanics, including ONH connective tissue microarchitecture and anatomy; intraocular pressure (IOP); and cerebrospinal fluid pressure (CSFp). We note that connective tissue factors can vary significantly from one individual to the next, as well as regionally within an eye, and that the understanding of ONH biomechanics is hindered by anatomical differences between small-animal models of glaucoma (rats and mice) and humans. Other challenges of using animal models of glaucoma to study the role of biomechanics include the complexity of assessing the degree of glaucomatous progression; and inadequate tools for monitoring and consistently elevating IOP in animal models. We conclude with a consideration of important open research questions/challenges in this area, including: (i) Creating a systems biology description of the ONH; (ii) addressing the role of astrocyte connective tissue remodeling and reactivity in glaucoma; (iii) providing a better characterization of ONH astrocytes and non-astrocytic constituent cells; (iv) better understanding the role of ONH astrocyte phagocytosis, proliferation and death; (v) collecting gene expression and phenotype data on a larger, more coordinated scale; and (vi) developing an implantable IOP sensor.

PMID:
28223180
PMCID:
PMC5438465
DOI:
10.1016/j.exer.2017.02.005
[Indexed for MEDLINE]
Free PMC Article

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