Autophagy in glaucoma: Crosstalk with apoptosis and its implications

Wang, Yao; Huang, Changquan; Zhang, Hongbing; Wu, Renyi

doi:10.1016/j.brainresbull.2015.06.001

Cited by 50 publications

(33 citation statements)

References 100 publications

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“…Autophagy is implicated in the pathogenesis of several neurodegenerative diseases, 85 and its complex role in the pathogenesis of glaucomatous damage is becoming a focus of emerging research. 86,87 Signaling of mTORC-1 is a major regulator of autophagy, and observations that in vivo inhibition may attenuate damage in animal models of neurodegeneration 88 has led to considerable interest in modulating this signaling pathway as a potential therapeutic intervention. Further investigation of the interactions between miR-27a and autophagy in the context of experimental glaucoma models is an area that merits further investigation.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression in the Glaucomatous Retina

Jayaram

Cepurna

Johnson

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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Section: Discussionmentioning

confidence: 99%

MicroRNA Expression in the Glaucomatous Retina

Jayaram

Cepurna

Johnson

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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“…Other autophagic regulatory signalling pathways include (1) eukaryotic initiation factor 2α(eIF2α), which responds to double-stranded RNA,nutrient deficiency, and endoplasmic reticulum (ER) stress; (2) 5'-AMP-activated protein kinase (AMPK), which responds to an increased AMP/ATP ratio and a low-energy environment bysuppressing mTORC1 signalling and activating autophagy through TSC1/2 phosphorylation; (3) BH3-only proteins, which contain a Bcl-2 homology-3 (BH3) domain, which interfere with Bcl-2/Bcl-X L -mediatedinhibition of the Beclin 1/class III PI3K complex; and (4) P62, which aberrantly accumulates in autophagy-deficient mice and interferes with the association of NRF2 and KEAP1, leading to NRF2 accumulation and stabilization 18-20. Additionally, the products of more than 20 yeast genes (the ATG genes) act downstream of TOR kinase, and these proteins have complicated functions, some of which remain unknown 3 (see Figure 1).…”

Section: Introduction To Autophagymentioning

confidence: 99%

The Evolving Functions of Autophagy in Ocular Health: A Double-edged Sword

Chai

Zhang

et al. 2016

Int. J. Biol. Sci.

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Autophagy plays an adaptive role in cell survival, development, differentiation and intracellular homeostasis. Autophagy is recognized as a 'self-cannibalizing' process that is active during stresses such as starvation, chemotherapy, infection, ageing, and oxygen shortage to protect organisms from various irritants and to regenerate materials and energy. However, autophagy can also lead to a form of programmed cell death distinct from apoptosis.Components of the autophagic pathway are constitutively expressed at a high level in the eye, including in the cornea, lens, retina, and orbit. In addition, the activation of autophagy is directly linked to the development of eye diseases such as age-related macular degeneration (ARMD), cataracts, diabetic retinopathy (DR), glaucoma, photoreceptor degeneration, ocular tumours, ocular infections and thyroid-associated ophthalmopathy (TAO). A high level of autophagy defends against external stress; however, excessive autophagy can result in deterioration, as observed in ocular diseases such as ARMD and DR.This review summarizes recent developments elucidating the relationship between autophagy and ocular diseases and the potential roles of autophagy in the pathogenesis and treatment of these diseases.

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“…The cytoprotective function of autophagy is activated in many circumstances by suppressing apoptosis [5]. It is now being recognized that autophagy is not only a survival response to growth factor or nutrient deprivation, but also an important mechanism underlying tumor cell suicide [6].…”

Section: Introductionmentioning

confidence: 99%

Berberine-induced autophagic cell death by elevating GRP78 levels in cancer cells

Zhang

Yang

et al. 2017

Oncotarget

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Berberine, an isoquinoline alkaloid extracted from Coptidis Rhizoma, has been shown to induce cancer cell autophagic death. Glucose regulated protein 78 (GRP78) is associated with stress-induced autophagy. However, the related mechanisms between berberine-induced cancer cell autophagy and GRP78 remain to be elucidated. Here, we report that berberine can induce autophagic cancer cell death by elevating levels of GRP78. These results further demonstrated that berberine enhanced GRP78 by suppression of ubiquitination / proteasomal degradation of GRP78 and activation of ATF6. Moreover, fluorescence spectrum assay revealed that berberine could bind to GRP78 and form complexes. Finally, co-IP analysis showed that the ability of GRP78 to bind to VPS34 was increased with berberine treatment. Taken together, our results suggest that berberine induces autophagic cancer cell death via enhancing GRP78 levels and the ability of GRP78 to bind to VPS34.

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Autophagy in glaucoma: Crosstalk with apoptosis and its implications

Cited by 50 publications

References 100 publications

MicroRNA Expression in the Glaucomatous Retina

MicroRNA Expression in the Glaucomatous Retina

The Evolving Functions of Autophagy in Ocular Health: A Double-edged Sword

Berberine-induced autophagic cell death by elevating GRP78 levels in cancer cells

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