Evidence map›Paper›PMID 24569607›Full record

ArticleEuropean journal of human genetics : EJHG2014

Cell therapy using retinal progenitor cells shows therapeutic effect in a chemically-induced rotenone mouse model of Leber hereditary optic neuropathy.

Fiona C Mansergh, Naomi Chadderton, Paul F Kenna, Oliviero L Gobbo, G Jane Farrar

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of human genetics : EJHG, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. [Effects of leptin on proliferation and differentiation of hypoxic rat retinal progenitor cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Fiona C ManserghOcular Genetics Unit, Smurfit Institute of Genetics, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland.
Naomi ChaddertonOcular Genetics Unit, Smurfit Institute of Genetics, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland.
Paul F Kenna1] Ocular Genetics Unit, Smurfit Institute of Genetics, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland [2] Research Foundation, The Royal Victoria Eye and Ear Hospital, Dublin, Ireland.
Oliviero L GobboSchool of Pharmacy and Pharmaceutical Sciences and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland.
G Jane FarrarOcular Genetics Unit, Smurfit Institute of Genetics, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland.
Trinity College Dublin · IE

Funding

Health Research Board MRCG/2007/9
6 · The paper itself

Abstract

Primary mitochondrial disorders occur at a prevalence of one in 10 000; ∼50% of these demonstrate ocular pathology. Leber hereditary optic neuropathy (LHON) is the most common primary mitochondrial disorder. LHON results from retinal ganglion cell pathology, which leads to optic nerve degeneration and blindness. Over 95% of cases result from one of the three common mutations in mitochondrial genes MTND1, MTND4 and MTND6, which encode elements of the complex I respiratory chain. Various therapies for LHON are in development, for example, intravitreal injection of adeno-associated virus carrying either the yeast NDI1 gene or a specific subunit of mammalian Complex I have shown visual improvement in animal models. Given the course of LHON, it is likely that in many cases prompt administration may be necessary before widespread cell death. An alternative approach for therapy may be the use of stem cells to protect visual function; this has been evaluated by us in a rotenone-induced model of LHON. Freshly dissected embryonic retinal cells do not integrate into the ganglion cell layer (GCL), unlike similarly obtained photoreceptor precursors. However, cultured retinal progenitor cells can integrate in close proximity to the GCL, and act to preserve retinal function as assessed by manganese-enhanced magnetic resonance imaging, optokinetic responses and ganglion cell counts. Cell therapies for LHON therefore represent a promising therapeutic approach, and may be of particular utility in treating more advanced disease.

Indexed as

AnimalsCell- and Tissue-Based TherapyCells, CulturedDependovirusDisease Models, AnimalElectron Transport Complex IGenetic MarkersMagnetic Resonance ImagingMiceMitochondriaMutationOptic Atrophy, Hereditary, LeberOptic NerveRetinaRetinal Ganglion CellsRotenoneElectron Transport Complex IGenetic MarkersNdi1 protein, S cerevisiaeRotenoneSaccharomyces cerevisiae Proteins

Identifiers

PMID24569607
PMCPMC4200438
OpenAlexW2034780448

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.