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Editors Selection IGR 8-3
Basic science: Accelerated aging of the trabecular meshworks
Comment by Douglas Rhee on:
12549 Cellular senescence in the glaucomatous outflow pathway, Liton PB; Challa P; Stinnett S et al., Experimental Gerontology, 2005; 40: 745-748
See also comment(s) by Ernst Tamm •The exact deficiency that underlies the elevated intraocular pressure in primary open-angle glaucoma is unknown. Evidence supports numerous potential pathophysiologies ranging from accumulations and alterations of extracellular matrix, trabecular meshwork cell dysfunction, and accelerated aging. In any one patient, some or all of these mechanisms may be active.
Trabecular meshwork (TM) cellularity decreases with age, and TM cells have a limited ability to divide. Cross-sectional studies showed that POAG patients have decreased TM cellularity compared with non-glaucomatous eyes. TM cells are necessary for the proper functioning of the trabecular meshwork. This has led to the hypothesis that accelerated aging may be the cause of elevated IOP. To further test this hypothesis, Liton et al. (778) compared the levels of senescence-associated-beta-galactosidase (SA-beta-gal), a marker for cellular senescence, in a group of six donor eyes from patients with POAG and 6 non-glaucomatous donor eyes.
Accelerated aging may contribute to the pathophysiology of glaucomaThey found a four-fold increase in the percentage of SA-beta-gal stained cells in POAG eyes compared to controls - particularily in the juxtacanalicular region. Although it is impossible to exclude the potential confounding effect of chronic anti-glaucoma medication use, their findings support the hypothesis that accelerated aging may contribute to the pathophysiology of glaucoma.
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