Evidence map›Paper›PMID 28055007›Full record

ArticleCell death & disease2017

Dysfunctional autophagy in RPE, a contributing factor in age-related macular degeneration.

Nady Golestaneh, Yi Chu, Yang-Yu Xiao, Gianna L Stoleru, Alexander C Theos

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed
27.2field-weighted citation impact, top 1% 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

244 citing papers in PubMed, 344 citations in OpenAlex.

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  10. Spontaneous whole retinal degeneration in aged Beclin1 heterozygous mice.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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  12. Fluorescence lifetime imaging ophthalmoscopy (FLIO) of patients with neovascular age-related macular degeneration before and after treatment with intravitreal ranibizumab.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
    Article
  13. Mapping the Hypoxic Fitness Landscape of Retinal Pigment Epithelial Cells.International journal of molecular sciences · 2026
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184 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

5 authors at 2 institutions in 1 country.

Nady GolestanehDepartment of Ophthalmology, Georgetown University Medical Center, Washington, DC, USA.
Yi ChuDepartment of Ophthalmology, Georgetown University Medical Center, Washington, DC, USA.
Yang-Yu XiaoDepartment of Ophthalmology, Georgetown University Medical Center, Washington, DC, USA.
Gianna L StoleruDepartment of Ophthalmology, Georgetown University Medical Center, Washington, DC, USA.
Alexander C TheosDepartment of Human Science, Georgetown University, Washington, DC, USA.
Georgetown University Medical Center · USGeorgetown University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a devastating neurodegenerative disease and a major cause of blindness in the developed world. Owing to its complexity and the lack of an adequate human model that recapitulates key aspects of the disease, the molecular mechanisms of AMD pathogenesis remain poorly understood. Here we show that cultured human retinal pigment epithelium (RPE) from AMD donors (AMD RPE) are functionally impaired and exhibit distinct phenotypes compared with RPE cultured from normal donors (normal RPE). Accumulation of lipid droplets and glycogen granules, disintegration of mitochondria, and an increase in autophagosomes were observed in AMD RPE cultures. Compared with normal RPE, AMD RPE exhibit increased susceptibility to oxidative stress, produce higher levels of reactive oxygen species (ROS) under stress conditions, and showed reduced mitochondrial activity. Measurement of the ratio of LC3-II/ LC3-I, revealed impaired autophagy in AMD RPE as compared with normal RPE. Autophagic flux was also reduced in AMD RPE as compared with normal RPE, as shown by inability of AMD RPE to downregulate p62 levels during starvation. Impaired autophagic pathways were further shown by analyzing late autophagic vesicles; immunostaining with lysosome-associated membrane protein 1 (LAMP-1) antibody revealed enlarged and annular LAMP-1-positive organelles in AMD RPE as opposed to smaller discrete puncta observed in normal RPE. Our study provides insights into AMD cellular and molecular mechanisms, proposes dysfunctional autophagy as an underlying mechanism contributing to the pathophysiology of the disease, and opens up new avenues for development of novel treatment strategies.

Indexed as

AutophagosomesCells, CulturedGlycogenHumansLipid DropletsLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMacular DegenerationMitochondriaOxidative StressReactive Oxygen SpeciesRetinal Pigment EpitheliumGlycogenLAMP1 protein, humanLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsReactive Oxygen Species

Identifiers

PMID28055007
PMCPMC5386365
OpenAlexW2569601267

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.