Evidence map›Paper›PMID 31007832›Full record

ArticleOxidative medicine and cellular longevity2019

Antimycin A-Induced Mitochondrial Damage Causes Human RPE Cell Death despite Activation of Autophagy.

Maria Hytti, Eveliina Korhonen, Juha M T Hyttinen, Heidi Roehrich, Kai Kaarniranta, Deborah A Ferrington, Anu Kauppinen

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

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  13. Overcoming amphotericin B resistance inAntimicrobial agents and chemotherapy · 2024
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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

7 authors at 2 institutions in 2 countries.

Maria HyttiSchool of Pharmacy, University of Eastern Finland, Kuopio, Finland.ORCID 0000-0003-2150-6847
Eveliina KorhonenSchool of Pharmacy, University of Eastern Finland, Kuopio, Finland.
Juha M T HyttinenSchool of Pharmacy, University of Eastern Finland, Kuopio, Finland.
Heidi RoehrichHistology Core for Vision Research, University of Minnesota, Minneapolis, MN, USA.
Kai KaarnirantaDepartment of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland.
Deborah A FerringtonDepartment of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, USA.
Anu KauppinenSchool of Pharmacy, University of Eastern Finland, Kuopio, Finland.ORCID 0000-0001-8254-0200
University of Eastern Finland · FIUniversity of Minnesota · US

Funding

Visual TestingP30EY011374 · NEI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NEWMAN, ERIC A · 1996 to 2019
$8.8M
NEI NIH HHS P30 EY011374
6 · The paper itself

Abstract

Mitochondrial dysfunction has been implicated in a wide variety of degenerative diseases, including age-related macular degeneration. Damage to mitochondria and mitochondrial DNA accumulates with age in the postmitotic retinal pigment epithelium (RPE), which could lead to RPE cell death and trigger disease. One possible mechanism for cells to avoid cell death is mitophagy, the targeted clearance of damaged mitochondria by autophagy. Here, we induced mitochondrial damage in human RPE cells (ARPE-19 and hRPE), using antimycin A, an inhibitor of complex III of the electron transport chain, and investigated cellular viability, mitochondrial structure and function, and autophagy activity. We observed that antimycin A evoked dose-dependent cell death, a rapid loss in mitochondrial membrane potential, and a collapse of oxidative phosphorylation. Mitochondria appeared swollen and there was clear damage to their cristae structure. At the same time, cells were undergoing active autophagy and were sensitive to autophagy inhibition by bafilomycin A1 or chloroquine. These results indicate that mitochondrial dysfunction can cause significant RPE damage and that autophagy is an important survival mechanism for cells suffering from mitochondrial damage.

Indexed as

AgedAntimycin AApoptosisAutophagyCell LineElectron TransportFemaleGlycolysisHumansMaleMembrane Potential, MitochondrialMitochondriaMitophagyOxidative PhosphorylationPhenotypeRetinal Pigment EpitheliumAntimycin A

Identifiers

PMID31007832
PMCPMC6441541
OpenAlexW2921478199

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.