Evidence map›Paper›PMID 27840061›Full record

ReviewExperimental eye research2017

Endogenous retinoic acid signaling is required for maintenance and regeneration of cornea.

Sandeep Kumar, Pascal Dollé, Norbert B Ghyselinck, Gregg Duester

Open access · greenAbstract readReview
In one paragraph

Review in Experimental eye research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Potential benefits of vitamin A and its derivatives in glaucoma.European journal of medical research · 2025
    Review
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  19. HCE-T cell line lacks cornea-specific differentiation markers compared to primary limbal epithelial cells and differentiated corneal epithelium.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020
    Article
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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 2 institutions in 2 countries.

Sandeep KumarDevelopment, Aging, and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA. Electronic address: sandeep@sbpdiscovery.org.
Pascal DolléInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France; Centre National de la Recherche Scientifique (CNRS), UMR 7104, Illkirch, France; Institut National de la Santé et de la Recherche Médicale (Inserm), U 964, Illkirch, France; Université de Strasbourg, Illkirch, France.
Norbert B GhyselinckInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France; Centre National de la Recherche Scientifique (CNRS), UMR 7104, Illkirch, France; Institut National de la Santé et de la Recherche Médicale (Inserm), U 964, Illkirch, France; Université de Strasbourg, Illkirch, France.
Gregg DuesterDevelopment, Aging, and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA. Electronic address: duester@sbpdiscovery.org.
Centre National de la Recherche Scientifique · FRSanford Burnham Prebys Medical Discovery Institute · US

Funding

Generation of Retinoid Signals During DevelopmentR01GM062848 · NIGMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI DUESTER, GREGG L · 2002 to 2015
$4.6M
NIGMS NIH HHS R01 GM062848
6 · The paper itself

Abstract

Retinoic acid (RA) is a biologically active metabolite of vitamin A (retinol) that serves as an important signaling molecule in orchestrating diverse developmental processes including multiple roles during ocular development. Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. However, it is unclear whether endogenous RA is required for maintenance and regeneration of adult cornea. Here, we investigated the role of Aldh1a genes in the adult cornea using a novel conditional Aldh1a1,2,3-flox/flox;Rosa26-CreERT2 loss-of-function mouse model to determine the biological function of RA. Our findings indicate that loss of RA synthesis results in corneal thinning characterized by reduced thickness of the stromal layer, impaired corneal epithelial cell proliferation, and increased apoptosis. Corneal thinning in Aldh1a-deficient mice was significantly rescued by RA administration, indicating an important role of endogenous RA signaling in adult corneal homeostasis and regeneration. Thus, Aldh1a1,2,3-flox/flox;Rosa26-CreERT2 mice provide a useful model for investigating the mechanistic role of RA signaling in adult corneal maintenance and could provide new insights into therapeutic approaches for controlling corneal repair to prevent vision loss.

Indexed as

ApoptosisAnimalsCell ProliferationEpithelium, CornealMiceRegenerationSignal TransductionTretinoinTretinoinALDH1ACorneal epitheliumCorneal stromaMouse genetic loss-of-functionRALDHRetinoic acid

Identifiers

PMID27840061
PMCPMC5363406
OpenAlexW2550974752

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.