Evidence map›Paper›PMID 31091656›Full record

ReviewInternational journal of molecular sciences2019

Role of Mitochondrial DNA Damage in ROS-Mediated Pathogenesis of Age-Related Macular Degeneration (AMD).

Kai Kaarniranta, Elzbieta Pawlowska, Joanna Szczepanska, Aleksandra Jablkowska, Janusz Blasiak

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 1 pooled it
21.6field-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

118 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

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58 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 2 countries.

Kai KaarnirantaDepartment of Ophthalmology, University of Eastern Finland, 70211 Kuopio, Finland. kai.kaarniranta@kuh.fi.ORCID 0000-0003-2600-8679
Elzbieta PawlowskaDepartment of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland. elzbieta.pawlowska@umed.lodz.pl.
Joanna SzczepanskaDepartment of Pediatric Dentistry, Medical University of Lodz, 92-216 Lodz, Poland. joanna.szczepanska@umed.lodz.pl.
Aleksandra JablkowskaDepartment of Infectious and Liver Diseases, W. Bieganski Hospital, 91-347 Lodz, Poland. jablkowska@pro.onet.pl.ORCID 0000-0001-9854-5233
Janusz BlasiakDepartment of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland. janusz.blasiak@biol.uni.lodz.pl.ORCID 0000-0001-9539-9584
Medical University of Lodz · PLGrochowski Hospital · PLUniversity of Eastern Finland · FIUniversity of Łódź · PL

Funding

National Science Centre, Poland 2017/27/B/NZ3/00872
6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a complex eye disease that affects millions of people worldwide and is the main reason for legal blindness and vision loss in the elderly in developed countries. Although the cause of AMD pathogenesis is not known, oxidative stress-related damage to retinal pigment epithelium (RPE) is considered an early event in AMD induction. However, the precise cause of such damage and of the induction of oxidative stress, including related oxidative effects occurring in RPE and the onset and progression of AMD, are not well understood. Many results point to mitochondria as a source of elevated levels of reactive oxygen species (ROS) in AMD. This ROS increase can be associated with aging and effects induced by other AMD risk factors and is correlated with damage to mitochondrial DNA. Therefore, mitochondrial DNA (mtDNA) damage can be an essential element of AMD pathogenesis. This is supported by many studies that show a greater susceptibility of mtDNA than nuclear DNA to DNA-damaging agents in AMD. Therefore, the mitochondrial DNA damage reaction (mtDDR) is important in AMD prevention and in slowing down its progression as is ROS-targeting AMD therapy. However, we know far less about mtDNA than its nuclear counterparts. Further research should measure DNA damage in order to compare it in mitochondria and the nucleus, as current methods have serious disadvantages.

Indexed as

DNA DamageAnimalsDNA, MitochondrialHumansMacular DegenerationReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Speciesage-related macular degenerationDNA damage responsemitochondriamtDNA damagereactive oxygen species

Identifiers

PMID31091656
PMCPMC6566654
OpenAlexW2946801360

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.