Evidence map›Paper›PMID 26854823›Full record

ArticleExperimental eye research2016

Increased retinal mtDNA damage in the CFH variant associated with age-related macular degeneration.

Deborah A Ferrington, Rebecca J Kapphahn, Michaela M Leary, Shari R Atilano, Marcia R Terluk, Pabalu Karunadharma, George Kuei-Jie Chen, Rinki Ratnapriya, Anand Swaroop, Sandra R Montezuma and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental eye research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.8field-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

60 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
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  6. QMRInternational journal of molecular sciences · 2025
    Article
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  8. Phase separation in mitochondrial fate and mitochondrial diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

11 authors at 3 institutions in 1 country.

Deborah A FerringtonDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, 55455, USA. Electronic address: ferri013@umn.edu.
Rebecca J KapphahnDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, 55455, USA.
Michaela M LearyDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, 55455, USA.
Shari R AtilanoGavin Herbert Eye Institute, University of California, Irvine, CA, 92697, USA.
Marcia R TerlukDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, 55455, USA.
Pabalu KarunadharmaDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, 55455, USA.
George Kuei-Jie ChenGavin Herbert Eye Institute, University of California, Irvine, CA, 92697, USA.
Rinki RatnapriyaNeurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, Bethesda, MD 20892, USA.
Anand SwaroopNeurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, Bethesda, MD 20892, USA.
Sandra R MontezumaDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, 55455, USA.
M Cristina KenneyGavin Herbert Eye Institute, University of California, Irvine, CA, 92697, USA.
University of Minnesota · USUniversity of California, Irvine · USNational Eye Institute · US

Funding

Mechanisms, modeling and therapies of retinal and macular neurodegenerationZIAEY000546 · NEI · NATIONAL EYE INSTITUTE · PI SWAROOP, ANAND · 2015 to 2025
$36.3M
University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
Training Grant: Functional Proteomics of AgingT32AG029796 · NIA · UNIVERSITY OF MINNESOTA · PI EDGAR A ARRIAGA, Douglas G Mashek · 2008 to 2026
$6.6M
NCATS NIH HHS UL1 TR001414NIA NIH HHS T32 AG029796
6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a major cause of blindness among the elderly in the developed world. Genetic analysis of AMD has identified 34 high-risk loci associated with AMD. The genes at these high risk loci belong to diverse biological pathways, suggesting different mechanisms leading to AMD pathogenesis. Thus, therapies targeting a single pathway for all AMD patients will likely not be universally effective. Recent evidence suggests defects in mitochondria (mt) of the retinal pigment epithelium (RPE) may constitute a key pathogenic event in some AMD patients. The purpose of this study is to determine if individuals with a specific genetic background have a greater propensity for mtDNA damage. We used human eyebank tissues from 76 donors with AMD and 42 age-matched controls to determine the extent of mtDNA damage in the RPE that was harvested from the macula using a long extension polymerase chain reaction assay. Genotype analyses were performed for ten common AMD-associated nuclear risk alleles (ARMS2, TNFRSF10A, CFH, C2, C3, APOE, CETP, LIPC, VEGF and COL10A1) and mtDNA haplogroups. Sufficient samples were available for genotype association with mtDNA damage for TNFRSF10A, CFH, CETP, VEGFA, and COL10A1. Our results show that AMD donors carrying the high risk allele for CFH (C) had significantly more mtDNA damage compared with donors having the wild-type genetic profile. The data from an additional 39 donors (12 controls and 27 AMD) genotyped for CFH alleles further supported these findings. Taken together, these studies provide the rationale for a more personalized approach for treating AMD by uncovering a significant correlation between the CFH high risk allele and accelerated mtDNA damage. Patients harboring this genetic risk factor may benefit from therapies that stabilize and protect the mt in the RPE.

Indexed as

DNA, MitochondrialRetinal Pigment EpitheliumAgedAged, 80 and overAllelesCase-Control StudiesComplement Factor HDNA DamageFemaleGenetic Predisposition to DiseaseGenotypeHumansMacular DegenerationMaleMiddle AgedPolymerase Chain ReactionComplement Factor HDNA, MitochondrialAge-related macular degenerationComplement factor HEyebank tissueHaplogroupsInflammationMitochondriamtDNA

Identifiers

PMID26854823
PMCPMC4842097
OpenAlexW2274104775

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.