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Article citations


Park, H.Y., Kim, J.H. and Park, C.K. (2012) Activation of Autophagy Induces Retinal Ganglion Cell Death in a Chronic Hypertensive Glaucoma Model. Cell Death & Disease, 3, e290.

has been cited by the following article:

  • TITLE: Identification of the Stress Which Causes Optineurin Aggregation

    AUTHORS: Satoshi Inagaki, Michinori Funato, Junko Seki, Chizuru Kawase, Kazuki Ohuchi, Shiori Ando, Shinsuke Nakamura, Masamitsu Shimazawa, Hideo Kaneko, Hideaki Hara

    KEYWORDS: Glaucoma, Induced Pluripotent Stem Cells, Retinal Ganglion Cells, Optineurin, Protein Aggregation

    JOURNAL NAME: Neuroscience and Medicine, Vol.10 No.2, June 10, 2019

    ABSTRACT: Glaucoma is a common neurodegenerative disease that can cause blindness and occurs worldwide. Currently, lowering intraocular pressure is the only therapy available to protect retinal ganglion cells (RGCs). However, this therapy does not prevent RGC death in all patients. Therefore, new therapeutic approaches for glaucoma are urgently required, and neuroprotection of RGCs is a focus for many researchers. Optineurin (OPTN) is one of the normal tension glaucoma (NTG) relative genes, while mutant OPTN can form a characteristic aggregation, causing RGC death. Hence, elucidation of the mechanism of OPTN aggregation might provide a clue to help understand RGC death. To examine whether non-mutant OPTN could also aggregate, we pharmacologically induced some glaucoma-related stresses, such as endoplasmic reticulum (ER) stress, glutamate toxicity, activation of TNF-α signaling, mitochondrial dysfunction, and autophagic flux impairment. Our results showed that ER stress, TNF-α signaling, and autophagic flux are involved in OPTN aggregation. Furthermore, our data indicated that increased ER stress, activation of TNF-α signaling, and impaired autophagic flux induce OPTN aggregation, suggesting that OPTN aggregation might be an important therapeutic target not only for familial NTG with mutated OPTN but also for patients with glaucoma more generally.