Journal
EXPERIMENTAL GERONTOLOGY
Volume 40, Issue 8-9, Pages 745-748Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2005.06.005
Keywords
trabecular meshwork; senescence; POAG; glaucoma; senescence-associated-beta-galactosidase
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Funding
- NEI NIH HHS [R01 EY016228, P30 EY005722, R01 EY016228-01A1, 1K23EY014019-01A1, K23 EY014019, P30 EY05722, EY01894, R01 EY001894] Funding Source: Medline
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The mechanisms responsible for the progressive malfunction of the trabecular meshwork (TM)-Schlemm's canal (SC) conventional outflow pathway tissue in primary open angle glaucoma (POAG) are still not fully understood. To determine whether POAG is characterized by an accumulation of senescent cells, similar to what has been described in other diseases, we have compared the levels of the senescence marker senescence-associated-beta-galactosidase (SA-beta-gal) in the outflow pathway cells of POAG and age-matched control donors. POAG donors demonstrated a statistically significant fourfold increase in the percentage of SA-beta-gal positive cells. These results suggest a potential role for cellular senescence in the pathophysiology of the outflow pathway. (c) 2005 Elsevier Inc. All rights reserved.
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