Light-Induced Retinal Ganglion Cell Damage and the Relevant Mechanisms

Zhao, Yuan; Shen, Ye

doi:10.1007/s10571-020-00819-0

Cited by 13 publications

(5 citation statements)

References 56 publications

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“…While the normal daily level of light (380-780 nm; 400-700 nm on primate' retinas) acts on the retina to induce vision and modulate circadian rhythms, excessive light has been reported to cause retinal cell death [108][109][110][111]. It was shown that light impinging on the retina could cause retinal cell death by interacting with mitochondrial constituents to generate reactive oxygen species (ROS) and trigger apoptosis [112,113].…”

Section: Retinal Light Damagementioning

confidence: 99%

Targeting Necroptosis: A Novel Therapeutic Option for Retinal Degenerative Diseases

Zhang¹,

Hu²,

Zhao³

et al. 2023

Int. J. Biol. Sci.

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The discovery of the necroptosis, a form of regulated necrosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed-lineage kinase domain-like pseudokinase (MLKL), represents a major breakthrough that has dramatically altered the conception of necrosis -traditionally thought of as uncontrolled cell death -in various human diseases. Retinal cell death is a leading cause of blindness and has been identified in most retinal diseases, e.g., age-related macular degeneration, glaucoma, retinal detachment, retinitis pigmentosa, etc. Increasing evidence demonstrates that retinal degenerative diseases also share a common mechanism in necroptosis. Exacerbated necroptotic cell death hinders the treatment for retinal degenerative diseases. In this review, we highlight recent advances in identifying retinal necroptosis, summarize the underlying mechanisms of necroptosis in retinal degenerative diseases, and discuss potential anti-necroptosis strategies, such as selective inhibitors and chemical agents, for treating retinal degenerative diseases.

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Section: Retinal Light Damagementioning

confidence: 99%

Targeting Necroptosis: A Novel Therapeutic Option for Retinal Degenerative Diseases

Zhang¹,

Hu²,

Zhao³

et al. 2023

Int. J. Biol. Sci.

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“…[ 2 ] Additionally, excessive light has adverse effects on retinal photoreceptor cells, retinal pigment epithelial (RPE) cells, and retinal ganglion cells (RGC). [ 3 ] Retinal photoreceptors are the key cells in visual phototransduction, which are located in the outer layer of the retina and transmit light stimuli from the optic nerve to the brain. [ 4 ] After light exposure, photoreceptor cells are initially damaged at the distal end of the rod out segment (ROS) which progresses over time to the entire ROS.…”

Section: Introductionmentioning

confidence: 99%

Changes in Cyclic Guanosine Monophosphate Channel of 661w Cells In vitro with Excessive Light Time

Zhang,

Yin,

Liu

2023

JOVR

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Purpose: To determine the response time and protective mechanism of the cyclic guanosine monophosphate (cGMP) channel in 661w cells. Methods: 661w cells were exposed to 4500Lux visible light for three and four days at the following exposure time periods per day: 20, 30, 60, 90, 120, and 180. Cells were incubated for the rest of the time without any other treatment. Cell activity and cell death rates were measured with Hoechst/PI (diphenylmethane/propidium iodide) staining. Western Blot was used to detect the levels of guanylate cyclase-activating proteins 1 (GCAP1), cGMP, and phosphodiesterase (PDE)6 in the cGMP-gated channel. Results: 661w cells showed low mortality within three days. The mortality rate increased from the fourth day, especially during the longer times (120 and 180 min) of light exposure. After three-day illumination, the level of cGMP increased after 20 and 90 min and the level of GCAP1 increased after 60 and 90 min. After four days of illumination, the level of GCAP1 upregulated after a time of 20 and 60 min, while the cGMP level decreased from 30 min. The expression of PDE6 upregulated at each light period. Conclusion: The survival rate of 661w cells was relevant to the time of light exposure. The changes in GCAP1, cGMP, and PDE6 levels over time were possibly related to cell metabolism and restoration after light-induced damage.

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“…The retina is the only fragile neuronal tissue that can sense light and produce visual signals to the brain. However, excessive and intensive light irradiation can lead to retinal light damage [ 1 , 2 ]. The retinal injury model for exposure to white light has been widely used in experimental research [ 3 – 7 ].…”

Section: Introductionmentioning

confidence: 99%

The Molecular Mechanism of Retina Light Injury Focusing on Damage from Short Wavelength Light

Fan

Zhang

Chi

et al. 2022

Oxidative Medicine and Cellular Longevity

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Natural visible light is an electromagnetic wave composed of a spectrum of monochromatic wavelengths, each with a characteristic color. Photons are the basic units of light, and their wavelength correlates to the energy of light; short-wavelength photons carry high energy. The retina is a fragile neuronal tissue that senses light and generates visual signals conducted to the brain. However, excessive and intensive light exposure will cause retinal light damage. Within the visible spectrum, short-wavelength light, such as blue light, carries higher energy, and thus the retinal injury, is more significant when exposed to these wavelengths. The damage mechanism triggered by different short-wavelength light varies due to photons carrying different energy and being absorbed by different photosensitive molecules in the retinal neurons. However, photooxidation might be a common molecular step to initiate cell death. Herein, we summarize the historical understanding of light, the key molecular steps related to retinal light injury, and the death pathways of photoreceptors to further decipher the molecular mechanism of retinal light injury and explore potential neuroprotective strategies.

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Light-Induced Retinal Ganglion Cell Damage and the Relevant Mechanisms

Cited by 13 publications

References 56 publications

Targeting Necroptosis: A Novel Therapeutic Option for Retinal Degenerative Diseases

Targeting Necroptosis: A Novel Therapeutic Option for Retinal Degenerative Diseases

Changes in Cyclic Guanosine Monophosphate Channel of 661w Cells In vitro with Excessive Light Time

The Molecular Mechanism of Retina Light Injury Focusing on Damage from Short Wavelength Light

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