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Review
. 2018 Feb 12;15(5):430-435.
doi: 10.7150/ijms.23428. eCollection 2018.

DJ-1 in Ocular Diseases: A Review

Cong Liu  1 , Xiufen Liu  1 , Jing Qi  1 , Om Prakash Pant  1 , Cheng-Wei Lu  1 , Jilong Hao  1
Affiliations
Review

DJ-1 in Ocular Diseases: A Review

Cong Liu et al. Int J Med Sci. .

Abstract

Protein deglycase DJ-1 (Parkinson disease protein 7) is a 20 kDa protein encoded by PARK7 gene. It is also known as a redox-sensitive chaperone and sensor that protect cells against oxidative stress-induced cell death in many human diseases. Though increasing evidence implicates that DJ-1 may also participate in ocular diseases, the overview of DJ-1 in ocular diseases remains elusive. In this review, we discuss the role as well as the underlying molecular mechanisms of DJ-1 in ocular diseases, including Fuchs endothelial corneal dystrophy (FECD), age-related macular degeneration (AMD), cataracts, and ocular neurodegenerative diseases, highlighting that DJ-1 may serve as a very striking therapeutic target for ocular diseases.

Keywords: DJ-1; ocular disease; oxidative stress.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Schematic diagram of DJ-1 regulation in ocular diseases. Under oxidative stress, the level of DJ-1 and Nrf2 are decreased in the cornea, causing the CECs apoptosis and leading to the reduction of FECD. DJ-1 and Nrf2 in the lens, resulting in the formation of a disulfide bond, crystal turbidity, and cataract formation. DJ-1 and Nrf2 are reduced in the retina, accelerating RPE degeneration and leading to AMD. Oxidative stress also induces the downregulation of Nrf2, DJ-1/PI3K/Akt and activation of ASK1, leading to the aggravation of irreversible RGCs apoptosis, resulting in ocular neurogeneration diseases. The expression level of DJ-1 in UM is significantly upregulated, DJ-1 protein may serve as a potential serum marker for UM.
See this image and copyright information in PMC

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