Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis.
Apoptosis
Corneal endothelium
Fuchs endothelial corneal dystrophy
Guttae
Mitochondria
Oxidative stress
Journal
Progress in retinal and eye research
ISSN: 1873-1635
Titre abrégé: Prog Retin Eye Res
Pays: England
ID NLM: 9431859
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
13
11
2019
revised:
05
04
2020
accepted:
10
04
2020
pubmed:
22
5
2020
medline:
30
10
2021
entrez:
22
5
2020
Statut:
ppublish
Résumé
Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto(mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.
Identifiants
pubmed: 32438095
pii: S1350-9462(20)30035-5
doi: 10.1016/j.preteyeres.2020.100863
pmc: PMC7648733
mid: NIHMS1597318
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
100863Subventions
Organisme : NEI NIH HHS
ID : P30 EY003790
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY020581
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
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