Evidence map›Paper›PMID 27607582›Full record

ArticleCell death & disease2016

Clearance of autophagy-associated dying retinal pigment epithelial cells - a possible source for inflammation in age-related macular degeneration.

M Szatmári-Tóth, E Kristóf, Z Veréb, S Akhtar, A Facskó, L Fésüs, A Kauppinen, K Kaarniranta, G Petrovski

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  7. Article
  8. Review
  9. Proteostasis in aging-associated ocular disease.Molecular aspects of medicine · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Role of Autophagy in Eye Diseases.Life (Basel, Switzerland) · 2021
    Review
  18. Article
  19. Review
  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

9 authors at 4 institutions in 4 countries.

M Szatmári-TóthDepartment of Biochemistry and Molecular Biology and MTA-DE Stem cell, Apoptosis and Genomics Research Group, University of Debrecen, Debrecen, Hungary.
E KristófDepartment of Biochemistry and Molecular Biology and MTA-DE Stem cell, Apoptosis and Genomics Research Group, University of Debrecen, Debrecen, Hungary.
Z VerébStem Cells and Eye Research Laboratory, Department of Ophthalmology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
S AkhtarDepartment of Optometry, College of Applied Medicine, King Saud University, Riyadh, Saudi Arabia.
A FacskóStem Cells and Eye Research Laboratory, Department of Ophthalmology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
L FésüsDepartment of Biochemistry and Molecular Biology and MTA-DE Stem cell, Apoptosis and Genomics Research Group, University of Debrecen, Debrecen, Hungary.
A KauppinenSchool of Pharmacy, Facility of Health Science, University of Eastern Finland, Kuopio, Finland.
K KaarnirantaSchool of Pharmacy, Facility of Health Science, University of Eastern Finland, Kuopio, Finland.
G PetrovskiDepartment of Biochemistry and Molecular Biology and MTA-DE Stem cell, Apoptosis and Genomics Research Group, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HUUniversity of Szeged · HUUniversity of Eastern Finland · FIKing Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinal pigment epithelial (RPE) cells can undergo different forms of cell death, including autophagy-associated cell death during age-related macular degeneration (AMD). Failure of macrophages or dendritic cells (DCs) to engulf the different dying cells in the retina may result in the accumulation of debris and progression of AMD. ARPE-19 and primary human RPE cells undergo autophagy-associated cell death upon serum depletion and oxidative stress induced by hydrogen peroxide (H2O2). Autophagy was revealed by elevated light-chain-3 II (LC3-II) expression and electron microscopy, while autophagic flux was confirmed by blocking the autophago-lysosomal fusion using chloroquine (CQ) in these cells. The autophagy-associated dying RPE cells were engulfed by human macrophages, DCs and living RPE cells in an increasing and time-dependent manner. Inhibition of autophagy by 3-methyladenine (3-MA) decreased the engulfment of the autophagy-associated dying cells by macrophages, whereas sorting out the GFP-LC3-positive/autophagic cell population or treatment by the glucocorticoid triamcinolone (TC) enhanced it. Increased amounts of IL-6 and IL-8 were released when autophagy-associated dying RPEs were engulfed by macrophages. Our data suggest that cells undergoing autophagy-associated cell death engage in clearance mechanisms guided by professional and non-professional phagocytes, which is accompanied by inflammation as part of an in vitro modeling of AMD pathogenesis.

Indexed as

AdenineAutophagyBiomarkersCell LineChloroquineCoculture TechniquesCulture Media, Serum-FreeGene ExpressionGenes, ReporterGreen Fluorescent ProteinsHumansHydrogen PeroxideInterleukin-6Interleukin-8MacrophagesMacular Degeneration3-methyladenineAdenineBiomarkersChloroquineCulture Media, Serum-FreeGreen Fluorescent ProteinsHydrogen PeroxideIL6 protein, humanInterleukin-6Interleukin-8MAP1LC3A protein, humanMicrotubule-Associated ProteinsTriamcinolone

Identifiers

PMID27607582
PMCPMC5059849
OpenAlexW2517700939

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.