Evidence map›Paper›PMID 17235687›Full record

ArticleJournal of clinical immunology2007

The role of anti-alpha-enolase autoantibodies in pathogenicity of autoimmune-mediated retinopathy.

Agnieszka Magrys, Thimmappa Anekonda, Gaoying Ren, Grazyna Adamus

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of clinical immunology, 2007. 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
2.7field-weighted citation impact, top 10% 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, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. [Relationship between anti-ENO1 antibody and systemic lupus erythematosus patients with retinopathy].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Moonlighting Proteins: The Case of the Hexokinases.Frontiers in molecular biosciences · 2021
    Review
  14. Review
  15. An update on autoimmune retinopathy.Indian journal of ophthalmology · 2020
    Review
  16. Review
  17. Detection of serum anti-retinal antibodies in the Chinese patients with presumed autoimmune retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019
    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

4 authors at 1 institution in 1 country.

Agnieszka MagrysNeurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon 97006, USA.
Thimmappa Anekonda
Gaoying Ren
Grazyna Adamus
Oregon Health & Science University · US

Funding

MECHANISM OF RETINAL DAMAGE IN AUTOIMMUNE RETINOPATHYR01EY013053 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ADAMUS, GRAZYNA · 1999 to 2008
$2.4M
NEI NIH HHS EY13053NEI NIH HHS R01 EY013053
6 · The paper itself

Abstract

Autoantibodies against alpha-enolase, a glycolytic enzyme, have been frequently associated with visual loss and retinal degeneration in patients with autoimmune and cancer-associated retinopathy; however their role in the pathogenicity of retinopathy has not been fully explained. Thus, we examined the causative role of anti-enolase antibodies on retinal cells. In the in vitro studies reported here, we found that Enol-1 monoclonal antibody against alpha-enolase significantly inhibited the catalytic function of enolase, which resulted in the depletion of glycolytic ATP. Enol-1 significantly increased intracellular Ca(2+), which led to Bax translocation to the mitochondria, and the release of cytochrome c into the cytoplasm--events that correlated with the initiation of apoptosis. Normal IgG did not induce intracellular calcium or reduce cytosolic ATP. L-type voltage-gated calcium channel blockers (nifedipine, D-cis-diltiazem, and verapamil) were effective in blocking the Ab-induced intracellular Ca(2+) rise and induction of Bax. Based on these findings we propose that chronic access of autoantibodies to the retina results in the inhibition of enolase catalytic function, depletion of ATP, and elevation in intracellular Ca(2+), leading to deregulation of glycolysis in retinal neurons and their destruction.

Indexed as

Adenosine TriphosphateAnimalsAntibodies, MonoclonalApoptosisAutoantibodiesAutoantigensBlotting, WesternCalciumCell LineGlycolysisNeuronsPhosphopyruvate HydrataseRatsRetinal DiseasesAdenosine TriphosphateAntibodies, MonoclonalAutoantibodiesAutoantigensCalciumPhosphopyruvate Hydratase

Identifiers

PMID17235687
OpenAlexW1969411640

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.