Evidence map›Paper›PMID 19447173›Full record

ArticleFree radical biology & medicine2009

Glutathione peroxidase 4 differentially regulates the release of apoptogenic proteins from mitochondria.

Hanyu Liang, Qitao Ran, Youngmok Charles Jang, Deborah Holstein, James Lechleiter, Tiffany McDonald-Marsh, Andrej Musatov, Wook Song, Holly Van Remmen, Arlan Richardson

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 86 citations in OpenAlex.

  1. Regulation of Glutathione Peroxidase 4 in Diabetic Retinopathy.International journal of molecular sciences · 2026
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  11. Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

10 authors at 4 institutions in 2 countries.

Hanyu LiangDepartment of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78245, USA.
Qitao Ran
Youngmok Charles Jang
Deborah Holstein
James Lechleiter
Tiffany McDonald-Marsh
Andrej Musatov
Wook Song
Holly Van Remmen
Arlan Richardson
The University of Texas Health Science Center at San Antonio · USGeriatric Research Education and Clinical Center · USSeoul National University of Education · KRSouth Texas Veterans Health Care System · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PETER J HORNSBY · 1995 to 2026
$30.6M
ROLE OF CASPASE-2 IN OSTEOCOLAST APOPTOSIS AGE-EePENDENT OSTEOPOROSISP01AG019316 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HERMAN, BRIAN A. · 2001 to 2011
$11.3M
TRANSGENIC ANIMAL CORE SUBCONTRACT WITH UTHSC AT SAN ANTONIOP01AG020591 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI BROOKS, SUSAN V · 2002 to 2014
$10.7M
Protein Oxidation as a Factor in the Mechanism of AgingR37AG026557 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RICHARDSON, ARLAN G. · 2005 to 2009
$1.2M
NIA NIH HHS 1P30-AG13319NIA NIH HHS P01 AG019316NIA NIH HHS P01 AG020591NIA NIH HHS P01AG020591NIA NIH HHS P01AG19316NIA NIH HHS P30 AG013319NIA NIH HHS R37 AG026557
6 · The paper itself

Abstract

Glutathione peroxidase 4 (Gpx4) is a unique antioxidant enzyme that repairs oxidative damage to biomembranes. In this study, we examined the effects of Gpx4 on the release of various apoptogenic proteins from mitochondria using transgenic mice overexpressing Gpx4 [Tg(GPX4(+/0))] and mice deficient in Gpx4 (Gpx4+/- mice). Diquat exposure triggered apoptosis that occurred through an intrinsic pathway and resulted in the mitochondrial release of cytochrome c (Cyt c), Smac/DIABLO, and Omi/HtrA2 in the liver of wild-type (Wt) mice. Liver apoptosis and Cyt c release were suppressed in Tg(GPX4(+/0)) mice but exacerbated in Gpx4+/- mice; however, neither the Tg(GPX4(+/0)) nor the Gpx4+/- mice showed any alterations in the levels of Smac/DIABLO or Omi/HtrA2 released from mitochondria. Submitochondrial fractionation data showed that Smac/DIABLO and Omi/HtrA2 existed primarily in the intermembrane space and matrix, whereas Cyt c and Gpx4 were both associated with the inner membrane. In addition, diquat exposure induced cardiolipin peroxidation in the liver of Wt mice; the levels of cardiolipin peroxidation were reduced in Tg(GPX4(+/0)) mice but elevated in Gpx4+/- mice. These data suggest that Gpx4 differentially regulates apoptogenic protein release owing to its inner membrane location in mitochondria and its ability to repair cardiolipin peroxidation.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCardiolipinsCarrier ProteinsCytochromes cDiquatGlutathione PeroxidaseHigh-Temperature Requirement A Serine Peptidase 2Lipid PeroxidationMiceMice, TransgenicMitochondria, LiverMitochondrial MembranesMitochondrial ProteinsPhospholipid Hydroperoxide Glutathione PeroxidaseApoptosis Regulatory ProteinsCardiolipinsCarrier ProteinsCytochromes cDiablo protein, mouseDiquatGlutathione PeroxidaseHigh-Temperature Requirement A Serine Peptidase 2Htra2 protein, mouseMitochondrial ProteinsPhospholipid Hydroperoxide Glutathione PeroxidaseSerine Endopeptidases

Identifiers

PMID19447173
PMCPMC2773016
OpenAlexW1993256031

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.