Evidence map›Paper›PMID 24346621›Full record

ReviewInvestigative ophthalmology & visual science2013

A perspective on the role of the extracellular matrix in progressive retinal degenerative disorders.

Muayyad R Al-Ubaidi, Muna I Naash, Shannon M Conley

Abstract readReview
In one paragraph

Review in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Article
  3. Fibrotic Changes in Rhegmatogenous Retinal Detachment.International journal of molecular sciences · 2025
    Review
  4. Expression of Versican in the Retina and Its Implication in Retinal Disease.Advances in experimental medicine and biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Retinal Metabolic Profile on IMPG2 Deficiency Mice with Subretinal Lesions.Advances in experimental medicine and biology · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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.

Muayyad R Al-UbaidiDepartment of Cell Biology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Muna I Naash
Shannon M Conley

Funding

Supplement for: Mechanism of Photoreceptor Cell Degeneration in Animal Models of Retinal DiseasesR01EY010609 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MUAYYAD R AL-UBAIDI, Muna I. Naash · 1995 to 2026
$11.0M
Compacted DNA Nanoparticles for Ocular TherapyR01EY018656 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI AL-UBAIDI, MUAYYAD R, NAASH, MUNA I. · 2008 to 2021
$5.6M
NEI NIH HHS R01 EY010609NEI NIH HHS R01 EY018656
6 · The paper itself

Abstract

Progressive inherited retinal degenerative disorders (PIRDDs) are the leading cause of blindness in developed countries, with AMD and RP constituting the majority of PIRDDs. Currently, over 8 million Americans have PIRDDs, and that number is estimated to drastically increase by the end of this decade. Although a mutant protein is expressed starting early during retinal development in patients with PIRDDs, symptoms of retinal degeneration do not manifest until much later. Historically, research has focused on understanding the role a mutation has in the function of a protein and what role the mutant protein has in the disease process. However, it remains unknown why the disease, irrespective of the mutation, manifests clinically much later in life, while cellular indicators of disease (e.g., accumulation of toxic protein products and cell death) occur throughout early and middle life. Herein, we propose that there exists a time point at which the degenerative process is accelerated, leading to the appearance of clinical symptoms. This point is defined by structural disruptions of the extracellular matrix (ECM). Death of a critical number of ECM-maintaining mutant protein-expressing retinal cells contributes to that break point in the degenerative process. Therefore, it is important to understand the changes occurring at the ECM during PIRDDs and to take that into account when therapeutic approaches are designed.

Indexed as

AgingRetinal DegenerationAnimalsDisease ProgressionExtracellular MatrixGenetic Predisposition to DiseaseGlobal HealthHumansIncidenceagingextracellular matrixretinal degeneration

Identifiers

PMID24346621
PMCPMC4587794

What OpenQuestion holds

Textmetadata
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.