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Clin Exp Ophthalmol. 2022 Jan 17; doi: 10.1111/ceo.14027. Epub 2022 Jan 17.

Pathogenesis of glaucoma: Extracellular matrix dysfunction in the trabecular meshwork-A review.

Clinical & experimental ophthalmology

Kate E Keller, Donna M Peters

Affiliations

  1. Casey Eye Institute, Oregon Health &Science University, Portland, Oregon, USA.
  2. Department of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine & Public Health, Madison, Wisconsin, USA.

PMID: 35037377 DOI: 10.1111/ceo.14027

Abstract

The trabecular meshwork regulates aqueous humour outflow from the anterior chamber of the eye. It does this by establishing a tunable outflow resistance, defined by the interplay between cells and their extracellular matrix (ECM) milieu, and the molecular interactions between ECM proteins. During normal tissue homeostasis, the ECM is remodelled and trabecular cell behaviour is modified, permitting increased aqueous fluid outflow to maintain intraocular pressure (IOP) within a relatively narrow physiological pressure. Dysfunction in the normal homeostatic process leads to increased outflow resistance and elevated IOP, which is a primary risk factor for glaucoma. This review delineates some of the changes in the ECM that lead to gross as well as some more subtle changes in the structure and function of the ECM, and their impact on trabecular cell behaviour. These changes are discussed in the context of outflow resistance and glaucoma.

© 2021 Royal Australian and New Zealand College of Ophthalmologists.

Keywords: extracellular matrix; glaucoma; trabecular meshwork

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