Evidence map›Paper›PMID 31901729›Full record

ArticleRedox biology2020

Peroxiredoxin-1 regulates lipid peroxidation in corneal endothelial cells.

Matthew Lovatt, Khadijah Adnan, Viridiana Kocaba, Martin Dirisamer, Gary S L Peh, Jodhbir S Mehta

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
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  9. A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells.Apoptosis : an international journal on programmed cell death · 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

6 authors at 4 institutions in 2 countries.

Matthew LovattTissue Engineering and Stem Cell Group, Singapore Eye Research Institute (SERI), Singapore; Duke-NUS Graduate Medical School, Ophthalmology & Visual Sciences Academic Clinical Programme (EYE ACP), Singapore. Electronic address: lovatt.matthew.jason@seri.com.sg.
Khadijah AdnanTissue Engineering and Stem Cell Group, Singapore Eye Research Institute (SERI), Singapore.
Viridiana KocabaTissue Engineering and Stem Cell Group, Singapore Eye Research Institute (SERI), Singapore.
Martin DirisamerUniversity Eye Hospital, Ludwig-Maximilian-University Munich, Germany.
Gary S L PehTissue Engineering and Stem Cell Group, Singapore Eye Research Institute (SERI), Singapore; Duke-NUS Graduate Medical School, Ophthalmology & Visual Sciences Academic Clinical Programme (EYE ACP), Singapore.
Jodhbir S MehtaTissue Engineering and Stem Cell Group, Singapore Eye Research Institute (SERI), Singapore; Duke-NUS Graduate Medical School, Ophthalmology & Visual Sciences Academic Clinical Programme (EYE ACP), Singapore; Singapore National Eye Centre (SNEC), Singapore; School of Material Science and Engineering, Nanyang Technological University, Singapore. Electronic address: Jodmehta@gmail.com.
Singapore Eye Research Institute · SGDuke-NUS Medical School · SGLudwig-Maximilians-Universität München · DESingapore National Eye Center · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Corneal transparency is maintained by a monolayer of corneal endothelial cells. Defects in corneal endothelial cells (CEnCs) can be rectified surgically through transplantation. Fuchs' endothelial corneal dystrophy (FECD) is the foremost cause of endothelial dysfunction and the leading indication for transplantation. Increased sensitivity of CEnCs to oxidative stress is thought to contribute to the pathogenesis of FECD through increased apoptosis. In part, this is thought to be due to loss of NRF2 expression: a global regulator of oxidative stress. We demonstrate that expression of the redox sensor, peroxiredoxin 1 (PRDX1) is selectively lost from CEnCs in FECD patient samples. We reveal that expression of PRDX1 is necessary to control the response of CEnCs to agents that cause lipid peroxidation. Iron-dependent lipid peroxidation drives non-apoptotic cell death termed ferroptosis. We establish that the inhibitor of ferroptosis, ferrostatin-1 rescues lipid peroxidation and cell death in CEnCs. Furthermore, we provide evidence that the transcription factor NRF2 similarly regulates lipid peroxidation in CEnCs.

Indexed as

Cell LineCell SurvivalCorneaCyclohexylaminesDown-RegulationEndothelial CellsFerroptosisFuchs' Endothelial DystrophyHumansIronLipid PeroxidationNF-E2-Related Factor 2Oxidative StressPeroxiredoxinsPhenylenediaminesCyclohexylaminesferrostatin-1IronNFE2L2 protein, humanNF-E2-Related Factor 2PeroxiredoxinsPhenylenediaminesPRDX1 protein, humanCorneal endothelial cellsFerroptosisFuchs' endothelial corneal dystrophyLipid peroxidationPRDX1

Identifiers

PMID31901729
PMCPMC6948265
OpenAlexW2998478599

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.