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Robert Hoerster, Mario Matthaei, Claus Cursiefen, Erdal Tahmaz, Thomas Streichert, Nasrin Refaian, Ludwig M Heindl; Ocular levels of angiotensin converting enzyme (ACE) in Fuchs’ Endothelial Dystrophy.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1355.
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Angiotensin converting enzyme (ACE) plays a pathogenetic role in fibrosis of several organs by promoting epithelial-mesenchymal-transition (EMT) via induction of TGF-beta expression. In Fuchs’ Endothelial Dystrophy (FED), EMT is suspected to cause fibrosis of Descemet’s membrane. We aimed to investigate the role of ACE in this process by analyzing ACE concentration levels in the aqueous humor of FED-patients in comparison to control cataract patients.
We obtained aqueous humor samples from patients receiving surgery for Cataract and FED (Descemet’s Membrane Endothelial Keratoplasty (DMEK)) respectively. All samples were stored at -80°C directly after extraction until analysis for no longer than 6 months. The Institute for Clinical Chemistry, University of Cologne analyzed the samples by a validated assay. Results are given in Units/l (U/l).
We included 34 samples from Cataract-patients and 10 samples from FED-patients. ACE concentrations were 0.57 ± 0.79 U/l (0-2.0) in the Cataract-group. In the FED-group we detected no ACE. This difference was statistically significant (P=0.034). We found no correlation of ACE concentrations with the amount of potential therapeutic systemic ACE-inhibition (ACE-I) for arterial hypertension (P=0.432, R=-0.192).
ACE-levels in aqueous humor are generally low and show great variability. Systemic intake of ACE-I does not seem to affect ocular ACE-levels. In FED-patients we did not detect any ACE in the aqueous humor. Further studies need to investigate if this finding is related to the pathogenesis of FED, and if ACE could be of therapeutic interest in FED.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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