机构:
Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA
Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USAHarvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA
Elhalis, Hussain
[1
,3
]
Azizi, Behrooz
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机构:
Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA
Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USAHarvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA
Azizi, Behrooz
[1
,3
]
Jurkunas, Ula V.
论文数: 0引用数: 0
h-index: 0
机构:
Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA
Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA 02114 USA
Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USAHarvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA
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
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.