Evidence map›Paper›PMID 22210054›Full record

ArticleFEBS letters2012

Mitochondria targeting of non-peroxidizable triphenylphosphonium conjugated oleic acid protects mouse embryonic cells against apoptosis: role of cardiolipin remodeling.

Yulia Y Tyurina, Muhammad A Tungekar, Mi-Yeon Jung, Vladimir A Tyurin, Joel S Greenberger, Detcho A Stoyanovsky, Valerian E Kagan

Abstract read
In one paragraph

Article in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review
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  10. Mitochondria and oxidative stress in heart aging.Age (Dordrecht, Netherlands) · 2016
    Review
  11. Article
  12. Article
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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 1 institution in 1 country.

Yulia Y TyurinaCenter for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA 15219, USA. yyt1@pitt.edu
Muhammad A Tungekar
Mi-Yeon Jung
Vladimir A Tyurin
Joel S Greenberger
Detcho A Stoyanovsky
Valerian E Kagan
University of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
Pulmonary Phosphatidylserine Oxidation in ApoptosisR01HL070755 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAGAN, VALERIAN E · 2002 to 2011
$3.0M
Lung Oxidative Stress/Inflammation By Carbon NanotubesR01OH008282 · OH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAGAN, VALERIAN E · 2005 to 2014
$2.8M
Oxygenated Species of Cardiolipins as Biomarkers of Mitochondrial DysfunctionR01ES020693 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAGAN, VALERIAN E, TYURINA, YULIA Y · 2011 to 2015
$1.7M
Irradiation Damage and Protection of Pulmonary Endothelium Oxidative LipidomicsR01HL094488 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAGAN, VALERIAN E · 2009 to 2010
$758k
NCATS NIH HHS UL1 TR000005NHLBI NIH HHS HL094488NHLBI NIH HHS HL70755NHLBI NIH HHS R01 HL070755NHLBI NIH HHS R01 HL094488NIAID NIH HHS U19 AI068021NIEHS NIH HHS ES020693NIEHS NIH HHS R01 ES020693NIOSH CDC HHS OH008282NIOSH CDC HHS R01 OH008282PHS HHS U19AIO68021
6 · The paper itself

Abstract

Peroxidation of cardiolipin in mitochondria is essential for the execution of apoptosis. We suggested that integration of oleic acid into cardiolipin generates non-oxidizable cardiolipin species hence protects cells against apoptosis. We synthesized mitochondria-targeted triphenylphosphonium oleic acid ester. Using lipidomics analysis we found that pretreatment of mouse embryonic cells with triphenylphosphonium oleic acid ester resulted in decreased contents of polyunsaturated cardiolipins and elevation of its species containing oleic acid residues. This caused suppression of apoptosis induced by actinomycin D. Triacsin C, an inhibitor of acyl-CoA synthase, blocked integration of oleic acid into cardiolipin and restored cell sensitivity to apoptosis.

Indexed as

AnimalsApoptosisCardiolipinsCell LineCytoprotectionDactinomycinEmbryo, MammalianMiceMitochondriaOleic AcidsOrganophosphorus CompoundsOxidation-ReductionTriazenesCardiolipinsDactinomycinOleic AcidsOrganophosphorus Compoundstriacsin CTriazenes

Identifiers

PMID22210054
PMCPMC3273856
OpenAlexW2008773559

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.