Evidence map›Paper›PMID 24707498›Full record

ReviewBioMed research international2014

Oxidative stress, hypoxia, and autophagy in the neovascular processes of age-related macular degeneration.

Janusz Blasiak, Goran Petrovski, Zoltán Veréb, Andrea Facskó, Kai Kaarniranta

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 3 pooled it
22.2field-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

146 citing papers in PubMed, 3 syntheses or guidelines pooled it, 250 citations in OpenAlex.

  1. Pooled it
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  3. ABCA1 rs1883025 polymorphism and risk of age-related macular degeneration.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2016
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86 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 4 institutions in 3 countries.

Janusz BlasiakFaculty of Biology and Environmental Protection, Department of Molecular Genetics, University of Lodz, 90-236 Lodz, Poland.ORCID 0000-0001-9539-9584
Goran PetrovskiDepartment of Ophthalmology, Faculty of Medicine, University of Szeged, Szeged 6720, Hungary ; Stem Cells and Eye Research Laboratory, Department of Biochemistry and Molecular Biology, Medical and Health Science Center and Apoptosis and Genomics Research Group of the Hungarian Academy of Sciences, University of Debrecen, Debrecen 4010, Hungary.ORCID 0000-0003-2905-9252
Zoltán VerébStem Cells and Eye Research Laboratory, Department of Biochemistry and Molecular Biology, Medical and Health Science Center and Apoptosis and Genomics Research Group of the Hungarian Academy of Sciences, University of Debrecen, Debrecen 4010, Hungary.
Andrea FacskóDepartment of Ophthalmology, Faculty of Medicine, University of Szeged, Szeged 6720, Hungary.
Kai KaarnirantaDepartment of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, 70211 Kuopio, Finland ; Department of Ophthalmology, Kuopio University Hospital, 70211 Kuopio, Finland.
University of Debrecen · HUUniversity of Eastern Finland · FIUniversity of Łódź · PLUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is the leading cause of severe and irreversible loss of vision in the elderly in developed countries. AMD is a complex chronic neurodegenerative disease associated with many environmental, lifestyle, and genetic factors. Oxidative stress and the production of reactive oxygen species (ROS) seem to play a pivotal role in AMD pathogenesis. It is known that the macula receives the highest blood flow of any tissue in the body when related to size, and anything that can reduce the rich blood supply can cause hypoxia, malfunction, or disease. Oxidative stress can affect both the lipid rich retinal outer segment structure and the light processing in the macula. The response to oxidative stress involves several cellular defense reactions, for example, increases in antioxidant production and proteolysis of damaged proteins. The imbalance between production of damaged cellular components and degradation leads to the accumulation of detrimental products, for example, intracellular lipofuscin and extracellular drusen. Autophagy is a central lysosomal clearance system that may play an important role in AMD development. There are many anatomical changes in retinal pigment epithelium (RPE), Bruch's membrane, and choriocapillaris in response to chronic oxidative stress, hypoxia, and disturbed autophagy and these are estimated to be crucial components in the pathology of neovascular processes in AMD.

Indexed as

AntioxidantsAutophagyHumansHypoxiaMacular DegenerationNeovascularization, PathologicOxidative StressReactive Oxygen SpeciesRetinal Pigment EpitheliumAntioxidantsReactive Oxygen Species

Identifiers

PMID24707498
PMCPMC3950832
OpenAlexW2021814263

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.