Evidence map›Paper›PMID 24732759›Full record

ReviewDevelopments in ophthalmology2014

General pathophysiology in retinal degeneration.

Katherine J Wert, Jonathan H Lin, Stephen H Tsang

Open access · greenAbstract readReview
In one paragraph

Review in Developments in ophthalmology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 86 citations in OpenAlex.

  1. Spontaneous whole retinal degeneration in aged Beclin1 heterozygous mice.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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  2. Review
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  12. Review
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  15. Frontiers in Understanding the Pathological Mechanism of Diabetic Retinopathy.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Review
  16. Article
  17. Review
  18. Retinal dystrophies: A look beyond the eyes.American journal of ophthalmology case reports · 2022
    Article
  19. Specialization of the photoreceptor transcriptome byProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Article
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 3 institutions in 2 countries.

Katherine J WertBernard and Shirlee Brown Glaucoma Laboratory, Departments of Ophthalmology, Pathology and Cell Biology, New York, N.Y., USA.
Jonathan H Lin
Stephen H Tsang
New York Hospital Queens · USUnité de Nutrition Humaine · FRUniversity of California, San Diego · US

Funding

Toward mechanism- and gene-based therapies for retinal degenerationR01EY018213 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Stephen H Tsang · 2008 to 2026
$6.6M
Vision Sciences Training GrantT32EY013933 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Carol A. Mason, CAROL M TROY · 2001 to 2026
$5.3M
Evaluating GWAS AMD Candidate Loci by Gene Editing in Human iPS CellsR21AG050437 · NIA · UNIVERSITY OF IOWA · PI BASSUK, ALEXANDER G, MAHAJAN, VINIT B · 2015 to 2016
$431k
NEI NIH HHS R01 EY018213NEI NIH HHS T32 EY013933NIA NIH HHS R21 AG050437
6 · The paper itself

Abstract

Retinal degeneration, including that seen in age-related macular degeneration and retinitis pigmentosa (RP), is the most common form of neural degenerative disease in the world. There is great genetic and allelic heterogeneity of the various retinal dystrophies. Classifications of these diseases can be ambiguous, as there are similar clinical presentations in retinal degenerations arising from different genetic mechanisms. As would be expected, alterations in the activity of the phototransduction cascade, such as changes affecting the renewal and shedding of the photoreceptor OS, visual transduction, and/or retinol metabolism have a great impact on the health of the retina. Mutations within any of the molecules responsible for these visual processes cause several types of retinal and retinal pigment epithelium degenerative diseases. Apoptosis has been implicated in the rod cell loss seen in a mouse model of RP, but the precise mechanisms that connect the activation of these pathways to the loss of phosphodiesterase (PDE6β) function has yet to be defined. Additionally, the activation of apoptosis by CCAAT/-enhancer-binding protein homologous protein (CHOP), after activation of the unfolded protein response pathway, may be responsible for cell death, although the mechanism remains unknown. However, the mechanisms of cell death after loss of function of PDE6, which is a commonly studied mammalian model in research, may be generalizable to loss of function of different key proteins involved in the phototransduction cascade.

Indexed as

ApoptosisGenetic Predisposition to DiseaseRetinal DegenerationVisual AcuityAnimalsEye ProteinsHumansPrognosisRetinal Ganglion CellsEye Proteins

Identifiers

PMID24732759
PMCPMC4405532
OpenAlexW1608860608

What OpenQuestion holds

Textmetadata
LicenceTDM
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.