Evidence map›Paper›PMID 29481912›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2018

Suppression of aberrant choroidal neovascularization through activation of the aryl hydrocarbon receptor.

Mayur Choudhary, Stephen Safe, Goldis Malek

Abstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. CD68: Potential Contributor to Inflammation and RPE Cell Dystrophy.Advances in experimental medicine and biology · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Gene Delivery of a Caspase Activation and Recruitment Domain Improves Retinal Pigment Epithelial Function and Modulates Inflammation in a Mouse Model with Features of Dry Age-Related Macular Degeneration.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2022
    Article
  7. Osteopontin accumulates in basal deposits of human eyes with age-related macular degeneration and may serve as a biomarker of aging.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Cell Line Authentication in Vision Research and Beyond: A Tale Retold.Investigative ophthalmology & visual science · 2020
    Article
  14. Review
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 at 2 institutions in 1 country.

Mayur ChoudharyDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, USA.
Stephen SafeVeterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA.
Goldis MalekDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, USA; Department of Pathology, Duke University School of Medicine, Durham, NC, USA. Electronic address: gmalek@duke.edu.
Duke University · USTexas A&M University · US

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
Lipid Activated Nuclear Receptors in Age-Related Macular DegenerationR01EY020868 · NEI · DUKE UNIVERSITY · PI MALEK, GOLDIS · 2011 to 2015
$1.8M
NEI NIH HHS P30 EY005722NEI NIH HHS R01 EY020868
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a ligand activated transcription factor, initially discovered for its role in regulating xenobiotic metabolism. There is extensive evidence supporting a multi-faceted role for AhR, modulating physiological pathways important in cell health and disease. Recently we demonstrated that the AhR plays a role in the pathogenesis of age-related macular degeneration (AMD), the leading cause of vision loss in the elderly. We found that loss of AhR exacerbates choroidal neovascular (CNV) lesion formation in a murine model. Herein we tested the therapeutic impact of AhR activation on CNV lesion formation and factors associated with aberrant neovascularization. We screened a panel of synthetic drugs and endogenous AhR ligands, assessed their ability to activate AhR in choroidal endothelial cells, and inhibit angiogenesis in vitro. Drugs with an anti-angiogenic profile were then administered to a murine model of CNV. Two compounds, leflunomide and flutamide, significantly inhibited CNV formation concurrent with positive modifying effects on angiogenesis, inflammation, extracellular matrix remodeling, and fibrosis. These results validate the role of the AhR pathway in regulating CNV pathogenesis, identify mechanisms of AhR-based therapies in the eye, and argue in favor of developing AhR as a drug target for the treatment of neovascular AMD.

Indexed as

AnimalsCell LineChoroidal NeovascularizationEndothelial CellsMacaca mulattaMacular DegenerationMiceMice, KnockoutReceptors, Aryl HydrocarbonReceptors, Aryl HydrocarbonAngiogenesisAryl hydrocarbon receptorChoroidal neovascularizationExtracellular matrixInflammationSelective receptor modulators

Identifiers

PMID29481912
PMCPMC5880720
OpenAlexW2791122177

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.