Evidence mapPaperPMID 39201313Full record

ReviewInternational journal of molecular sciences2024

Mitochondria in Retinal Ganglion Cells: Unraveling the Metabolic Nexus and Oxidative Stress.

Tsai-Hsuan Yang, Eugene Yu-Chuan Kang, Pei-Hsuan Lin, Benjamin Ben-Chi Yu, Jason Hung-Hsuan Wang, Vincent Chen, Nan-Kai Wang

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed.

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  19. Neuroprotection in Diabetes Retinal Disease: An Unmet Medical Need.International journal of molecular sciences · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Tsai-Hsuan YangDepartment of Education, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan 33305, Taiwan.ORCID 0009-0003-5932-611X
Eugene Yu-Chuan KangDepartment of Ophthalmology, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan 33305, Taiwan.ORCID 0000-0001-6814-6530
Pei-Hsuan LinDepartment of Ophthalmology, Edward S. Harkness Eye Institute, Columbia University Irving Medical Center, Columbia University, New York, NY 10032, USA.
Benjamin Ben-Chi YuFu Foundation School of Engineering & Applied Science, Columbia University, New York, NY 10027, USA.ORCID 0009-0009-2938-5593
Jason Hung-Hsuan WangDepartment of Ophthalmology, Edward S. Harkness Eye Institute, Columbia University Irving Medical Center, Columbia University, New York, NY 10032, USA.
Vincent ChenDepartment of Ophthalmology, Edward S. Harkness Eye Institute, Columbia University Irving Medical Center, Columbia University, New York, NY 10032, USA.ORCID 0009-0003-7120-4449
Nan-Kai WangDepartment of Ophthalmology, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan 33305, Taiwan.ORCID 0000-0002-6277-9879

Funding

Gerstner Philanthropies grantsNational Eye Institute of the National Institutes of Health Award Number R01EY031354 and 5P30EY019007NEI NIH HHS P30 EY019007NEI NIH HHS R01 EY031354Research to Prevent Blindness, New York, NY an Unrestricted Grant to the Department of Ophthalmology, Columbia UniversityThe Vagelos College of Physicians & Surgeons (VP&S) grants
6 · The paper itself

Abstract

This review explored the role of mitochondria in retinal ganglion cells (RGCs), which are essential for visual processing. Mitochondrial dysfunction is a key factor in the pathogenesis of various vision-related disorders, including glaucoma, hereditary optic neuropathy, and age-related macular degeneration. This review highlighted the critical role of mitochondria in RGCs, which provide metabolic support, regulate cellular health, and respond to cellular stress while also producing reactive oxygen species (ROS) that can damage cellular components. Maintaining mitochondrial function is essential for meeting RGCs' high metabolic demands and ensuring redox homeostasis, which is crucial for their proper function and visual health. Oxidative stress, exacerbated by factors like elevated intraocular pressure and environmental factors, contributes to diseases such as glaucoma and age-related vision loss by triggering cellular damage pathways. Strategies targeting mitochondrial function or bolstering antioxidant defenses include mitochondrial-based therapies, gene therapies, and mitochondrial transplantation. These advances can offer potential strategies for addressing mitochondrial dysfunction in the retina, with implications that extend beyond ocular diseases.

Indexed as

MitochondriaOxidative StressRetinal Ganglion CellsAnimalsGlaucomaHumansReactive Oxygen SpeciesReactive Oxygen Speciesantioxidantsautosomal dominant optic atrophygene therapyglaucomametabolismmitochondriamitochondrial transplantationoxidative stressretinal ganglion cellsretinopathy

Identifiers

PMID39201313
PMCPMC11354650

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.