Evidence map›Paper›PMID 29367744›Full record

ArticleCell death & disease2018

Overexpression of parkin protects retinal ganglion cells in experimental glaucoma.

Yi Dai, Xinxin Hu, Xinghuai Sun

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
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

51 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  11. Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. The role of RGC degeneration in the pathogenesis of glaucoma.International journal of biological sciences · 2025
    Review
  17. Protein misfolding and mitochondrial dysfunction in glaucoma.Frontiers in cell and developmental biology · 2025
    Review
  18. Article
  19. Article
  20. Review
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

3 authors at 2 institutions in 2 countries.

Yi DaiDepartment of Ophthalmology and Vision Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. ydai@fudan.edu.cn.
Xinxin HuDepartment of Ophthalmology and Vision Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Xinghuai SunDepartment of Ophthalmology and Vision Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Eye & ENT Hospital of Fudan University · CNMinistry of Health · OM

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma is a leading cause of irreversible blindness and characterized by progressive damage of retinal ganglion cells (RGCs). Growing evidences have linked impaired mitophagy with neurodegenerative diseases, while the E3 ubiquitin ligase parkin may play a key role. However, the pathophysiological relationship between parkin and glaucoma remains largely unknown. Using chronic hypertensive glaucoma rats induced by translimbal laser photocoagulation, we show here that the protein level of parkin and its downstream optineurin proteins were increased in hypertensive retinas. The ratio of LC3-II to LC3-I, the number of mitophagosomes, and unhealthy mitochondria were increased in hypertensive optic nerves. Overexpression of parkin by viral vectors increased RGC survival in glaucomatous rats in vivo and under excitotoxicity in vitro. It also promoted optineurin expression and improved mitochondrial health. In parkin-overexpressed glaucomatous rats, the ratio of LC3-II to LC3-I, LAMP1 level, and the number of mitophagosomes in optic nerve were decreased at 3 days, yet increased at 2 weeks following intraocular pressure (IOP) elevation. These findings demonstrate that dysfunction of mitophagy exist in RGCs of glaucomatous rats. Overexpression of parkin exerted a significant protective effect on RGCs and partially restored dysfunction of mitophagy in response to cumulative IOP elevation.

Indexed as

NeuroprotectionAnimalsCell SurvivalChronic DiseaseEpendymoglial CellsGlaucomaGlial Fibrillary Acidic ProteinGlutamatesHypertensionIntraocular PressureLysosomal-Associated Membrane Protein 1MaleMitochondriaMitophagyNeurotoxinsOptic NerveGlial Fibrillary Acidic ProteinGlutamatesLysosomal-Associated Membrane Protein 1NeurotoxinsOPTN protein, ratparkin proteinTranscription Factor TFIIIAUbiquitin-Protein Ligases

Identifiers

PMID29367744
PMCPMC5833378
OpenAlexW2793407457

What OpenQuestion holds

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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 OpenQuestion graph.