Protective effect of heat shock protein 70 on glaucomatous optic nerve injury

Authors: Chen Di,  Guo Wenyi

DOI: 10.3760/cma.j.issn.2095-0160.2019.06.015
Published 2019-06-10
Cite as Chin J Exp Ophthalmol, 2019,37(6): 477-480.

Abstract                               [View PDF] [Read Full Text]

Glaucoma is characterized by progressive loss of vision, which is caused by degeneration of retinal ganglion cells (RGCs). Heat shock proteins (HSP), whose expression could be induced by a variety of stressful stimuli, belong to a superfamily of stress proteins.Cell protective roles of HSPs are related to their chaperone functions, antiapoptotic and antinecrotic effects.In recent years, gene polymorphism studies have shown that changes in HSP70 expression are associated with primary angle-closure glaucoma and open angle glaucoma.Furthermore, emerging evidence reveals that HSP70 plays an important role in the protection of optic nerve, RGCs and trabecular meshwork cells.Animal experiment studies have shown that virus transfection, teprenone and HSP90 inhibitor 17-AAG could artificially induce the expression of HSP70 in vivo and prevent glaucomatous optic nerve from injury.These evidences provide new ideas of glaucoma treatment.This article aimed to review the current research progress of HSP70 in the pathogenesis, progression and treatment of glaucoma.

Key words:

Glaucoma; Heat shock protein 70; Retinal ganglion cells

Contributor Information

Chen Di
Department of Ophthalmology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine; Institute of Ophthalmology and Visual Science, Shanghai Jiao Tong University School of Medicine; Jiuyuan Medical School, Shanghai Jiao Tong University, Shanghai 200011, China
Guo Wenyi
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