Evidence map›Paper›PMID 31226340›Full record

ArticleExperimental eye research2019

Age-related macular degeneration (AMD) mitochondria modulate epigenetic mechanisms in retinal pigment epithelial cells.

Sonali Nashine, Anthony B Nesburn, Baruch D Kuppermann, M Cristina Kenney

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Contemporary insights into elamipretide's mitochondrial mechanism of action and therapeutic effects.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Sonali NashineDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA, USA.
Anthony B NesburnDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA, USA; Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Baruch D KuppermannDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA, USA.
M Cristina KenneyDepartment of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA, USA; Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA, USA. Electronic address: mkenney@uci.edu.
University of California, Irvine · USCedars-Sinai Medical Center · US

Funding

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
METALLOPROTEINASES IN NORMAL &KERATOCONUS CORNEASR01EY006807 · NEI · UNIVERSITY OF CALIFORNIA IRVINE · PI KENNEY, MARIA C · 1987 to 2003
$1.3M
Protective Effects of Humanin on AMD MitochondriaR01EY027363 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KENNEY, MARIA C · 2019 to 2021
$1.2M
NCATS NIH HHS UL1 TR001414NEI NIH HHS R01 EY006807NEI NIH HHS R01 EY027363
6 · The paper itself

Abstract

Mitochondrial damage and epigenetic modifications have been implicated in the pathogenesis of Age-related Macular Degeneration (AMD). This study was designed to investigate the effects of AMD/normal mitochondria on epigenetic regulation in human transmitochondrial retinal pigment epithelial (RPE) cells in vitro. Human RPE cybrid cell lines were created by fusing mitochondria-deficient (Rho0) ARPE-19 cells with platelets obtained from either AMD patients (AMD cybrids) or normal subjects (normal cybrids). Therefore, all cybrids had identical nuclei (derived from ARPE-19 cells) but mitochondria derived from either AMD patients or age-matched normal subjects. AMD cybrids demonstrated increased RNA/protein levels for five methylation-related and four acetylation-related genes, along with lower levels of two methylation and three acetylation genes compared to normal cybrids. Demethylation using 5-Aza-2'-deoxycytidine (DAC) led to decreased expression of VEGF-A gene in AMD cells. Trichostatin A (TSA), an HDAC inhibitor, also influenced protein levels of VEGF-A, HIF1α, NFκB, and CFH in AMD cells. Our findings suggest that retrograde signaling leads to mitochondria-nucleus interactions that influence the epigenetic status of the RPE cells and this may help in the identification of future potential therapeutic targets for AMD.

Indexed as

Epigenesis, GeneticCell NucleusCells, CulturedDNA MethylationDNA, MitochondrialGene Expression RegulationGenome, MitochondrialHumansMacular DegenerationMitochondriaRetinal Pigment EpitheliumSignal TransductionVascular Endothelial Growth Factor ADNA, MitochondrialVascular Endothelial Growth Factor AAcetylationAge-related macular degenerationAMDAMD mitochondriaEpigeneticsMethylation

Identifiers

PMID31226340
PMCPMC7192350
OpenAlexW2952828998

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.