Evidence map›Paper›PMID 25392995›Full record

ArticlePloS one2014

Identification of a common non-apoptotic cell death mechanism in hereditary retinal degeneration.

Blanca Arango-Gonzalez, Dragana Trifunović, Ayse Sahaboglu, Katharina Kranz, Stylianos Michalakis, Pietro Farinelli, Susanne Koch, Fred Koch, Sandra Cottet, Ulrike Janssen-Bienhold and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

137 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Restoring Sight: The Journey of AIPL1 from Discovery to Therapy.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. ZebrafishInternational journal of molecular sciences · 2025
    Article
  15. Article
  16. Review
  17. PARP inhibition preserves cone photoreceptors in rd2 retina.Acta neuropathologica communications · 2025
    Article
  18. Article
  19. Article
  20. Exploring Histone Modifications in Inherited Retinal Disorders.Advances in experimental medicine and biology · 2025
    Review

77 more citing papers are in PubMed but not listed here.

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

17 authors at 5 institutions in 3 countries.

Blanca Arango-GonzalezInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany.
Dragana TrifunovićInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany.
Ayse SahabogluInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany.
Katharina KranzDepartment of Neurobiology, University of Oldenburg, Oldenburg, Germany.
Stylianos MichalakisCenter for Integrated Protein Science Munich and Department of Pharmacy - Center for Drug Research, Ludwig-Maximilians-University Munich, Munich, Germany.
Pietro FarinelliInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany; Division of Ophthalmology, Department of Clinical Sciences, University of Lund, Lund, Sweden.
Susanne KochCenter for Integrated Protein Science Munich and Department of Pharmacy - Center for Drug Research, Ludwig-Maximilians-University Munich, Munich, Germany.
Fred KochCenter for Integrated Protein Science Munich and Department of Pharmacy - Center for Drug Research, Ludwig-Maximilians-University Munich, Munich, Germany.
Sandra CottetInstitute for Research in Ophthalmology, Sion, Switzerland.
Ulrike Janssen-BienholdDepartment of Neurobiology, University of Oldenburg, Oldenburg, Germany.
Karin DedekDepartment of Neurobiology, University of Oldenburg, Oldenburg, Germany.
Martin BielCenter for Integrated Protein Science Munich and Department of Pharmacy - Center for Drug Research, Ludwig-Maximilians-University Munich, Munich, Germany.
Eberhart ZrennerInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany; Centre for Integrative Neuroscience, University of Tuebingen, Tuebingen, Germany.
Thomas EulerInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany; Centre for Integrative Neuroscience, University of Tuebingen, Tuebingen, Germany.
Per EkströmDivision of Ophthalmology, Department of Clinical Sciences, University of Lund, Lund, Sweden.
Marius UeffingInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany.
François Paquet-DurandInstitute for Ophthalmic Research, University of Tuebingen, Tuebingen, Germany.
University of Tübingen · DELudwig-Maximilians-Universität München · DECarl von Ossietzky Universität Oldenburg · DELund University · SEInstitut de Recherche en Opthalmologie · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell death in neurodegenerative diseases is often thought to be governed by apoptosis; however, an increasing body of evidence suggests the involvement of alternative cell death mechanisms in neuronal degeneration. We studied retinal neurodegeneration using 10 different animal models, covering all major groups of hereditary human blindness (rd1, rd2, rd10, Cngb1 KO, Rho KO, S334ter, P23H, Cnga3 KO, cpfl1, Rpe65 KO), by investigating metabolic processes relevant for different forms of cell death. We show that apoptosis plays only a minor role in the inherited forms of retinal neurodegeneration studied, where instead, a non-apoptotic degenerative mechanism common to all mutants is of major importance. Hallmark features of this pathway are activation of histone deacetylase, poly-ADP-ribose-polymerase, and calpain, as well as accumulation of cyclic guanosine monophosphate and poly-ADP-ribose. Our work thus demonstrates the prevalence of alternative cell death mechanisms in inherited retinal degeneration and provides a rational basis for the design of mutation-independent treatments.

Indexed as

AnimalsAnimals, Genetically ModifiedCalpainCell DeathCyclic GMPDisease Models, AnimalHistone DeacetylasesLight Signal TransductionMiceMutationPoly Adenosine Diphosphate RibosePoly(ADP-ribose) PolymerasesRatsRetinal DegenerationCalpainCyclic GMPHistone DeacetylasesPoly Adenosine Diphosphate RibosePoly(ADP-ribose) Polymerases

Identifiers

PMID25392995
PMCPMC4230983
OpenAlexW2077799422

What OpenQuestion 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 OpenQuestion graph.