Fuchs Endothelial Corneal Dystrophy

被引：171

作者：

Elhalis, Hussain ^{[1
,3
]}

Azizi, Behrooz ^{[1
,3
]}

Jurkunas, Ula V. ^{[1
,2
,3
]}

机构：

[1] Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA

[2] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA 02114 USA

[3] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA

来源：

OCULAR SURFACE | 2010年 / 8卷 / 04期

关键词：

antioxidants; apoptosis; collagen VIII; corneal endothelium; Fuchs endothelial corneal dystrophy; genetics; oxidative stress; proteomics; GROWTH-FACTOR-BETA; THIOL-SPECIFIC ANTIOXIDANT; INDUCED PROTEIN TGFBIP; DESCEMETS-MEMBRANE; OXIDATIVE STRESS; INTERSTITIAL KERATITIS; PEROXIREDOXIN SUBTYPES; CLUSTERIN EXPRESSION; ALZHEIMERS-DISEASE; EPITHELIAL-CELLS;

D O I：

10.1016/S1542-0124(12)70232-X

中图分类号：

R77 [眼科学];

学科分类号：

100212 ;

摘要：

Fuchs endothelial corneal dystrophy (FECD) Is characterized by progressive loss of corneal endothelial cells, thickening of Descement's membrane and deposition of extracellular matrix in the form of guttae. When the number of endothelial cells becomes critically low, the cornea swells and causes loss of vision. The clinical course of FECD usually spans 10-20 years. Corneal transplantation is currently the only modality used to restore vision. Over the last several decades genetic studies have detected several genes, as well as areas of chromosomal loci associated with the disease. Proteomic studies have given rise to several hypotheses regarding the pathogenesis of FECD. This review expands upon the recent findings from proteomic and genetic studies and builds upon recent advances in understanding the causes of this common corneal disorder.

引用

页码：173 / 184

页数：12

共 111 条

[1]

ABBOTT RL, 1981, OPHTHALMOLOGY, V88, P788

[2] FUCHS ENDOTHELIAL DYSTROPHY OF THE CORNEA [J].

ADAMIS, AP ;

FILATOV, V ;

TRIPATHI, BJ ;

TRIPATHI, RC .

SURVEY OF OPHTHALMOLOGY, 1993, 38 (02) :149-168

[3] Genome-wide Linkage Scan in Fuchs Endothelial Corneal Dystrophy [J].

Afshari, Natalie A. ;

Li, Yi-Ju ;

Pericak-Vance, Margaret A. ;

Gregory, Simon ;

Klintworth, Gordon K. .

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 2009, 50 (03) :1093-1097

[4] No pathogenic mutations identified in the COL8A1 and COL8A2 genes in familial Fuchs corneal dystrophy [J].

Aldave, Anthony J. ;

Rayner, Sylvia A. ;

Salem, Andrew K. ;

Yoo, Gina L. ;

Kim, Brian T. ;

Saeedian, Monika ;

Sonmez, Baris ;

Yellore, Vivek S. .

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 2006, 47 (09) :3787-3790

[5]

Arffa RC, 1991, GRAYSONS DIS CORNEA

[6] APOPTOSIS INDUCED BY INHIBITION OF INTERCELLULAR CONTACT [J].

BATES, RC ;

BURET, A ;

VANHELDEN, DF ;

HORTON, MA ;

BURNS, GF .

JOURNAL OF CELL BIOLOGY, 1994, 125 (02) :403-415

[7]

BECKER B, 1976, DIAGNOSIS THERAPY GL, P265

[8] Fuchs' endothelial dystrophy: a fresh look at an aging disease [J].

Bergmanson, JPG ;

Sheldon, TM ;

Goosey, JD .

OPHTHALMIC AND PHYSIOLOGICAL OPTICS, 1999, 19 (03) :210-222

[9] The transforming growth factor-β-inducibie matrix protein βig-h3 interacts with fibronectin [J].

Billings, PC ;

Whitbeck, JC ;

Adams, CS ;

Abrams, WR ;

Cohen, AJ ;

Engelsberg, BN ;

Howard, PS ;

Rosenbloom, J .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (31) :28003-28009

[10] Missense mutations in COL8A2, the gene encoding the α2 chain of type VIII collagen, cause two forms of corneal endothelial dystrophy [J].

Biswas, S ;

Munier, FL ;

Yardley, J ;

Hart-Holden, N ;

Perveen, R ;

Cousin, P ;

Sutphin, JE ;

Noble, B ;

Batterbury, M ;

Kielty, C ;

Hackett, A ;

Bonshek, R ;

Ridgway, A ;

McLeod, D ;

Sheffield, VC ;

Stone, EM ;

Schorderet, DF ;

Black, GCM .

HUMAN MOLECULAR GENETICS, 2001, 10 (21) :2415-2423

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