Evidence map›Paper›PMID 27725964›Full record

ArticleACS central science2016

A Mitochondrial-Targeted Nitroxide Is a Potent Inhibitor of Ferroptosis.

Tanja Krainz, Michael M Gaschler, Chaemin Lim, Joshua R Sacher, Brent R Stockwell, Peter Wipf

Abstract read
In one paragraph

Article in ACS central science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
–field-weighted citation impact
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

133 citing papers in PubMed.

  1. Review
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  6. Ferroptosis inhibitors: mechanisms of action and therapeutic potential.Cellular and molecular life sciences : CMLS · 2025
    Review
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  8. Review
  9. Review
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  11. Ferroptosis in cancer: revealing the multifaceted functions of mitochondria.Cellular and molecular life sciences : CMLS · 2025
    Review
  12. Review
  13. Article
  14. Article
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  16. Article
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73 more citing papers are in PubMed but not listed here.

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.

Tanja KrainzDepartment of Chemistry, University of Pittsburgh , 219 Parkman Avenue, Pittsburgh, Pennsylvania 15260, United States.
Michael M GaschlerDepartment of Biological Sciences and Department of Chemistry, Columbia University , 550 West 120th Street, Northwest Corner Building, MC 4846, New York, New York 10027, United States.
Chaemin LimDepartment of Chemistry, University of Pittsburgh , 219 Parkman Avenue, Pittsburgh, Pennsylvania 15260, United States.
Joshua R SacherDepartment of Chemistry, University of Pittsburgh , 219 Parkman Avenue, Pittsburgh, Pennsylvania 15260, United States.
Brent R StockwellDepartment of Biological Sciences and Department of Chemistry, Columbia University, 550 West 120th Street, Northwest Corner Building, MC 4846, New York, New York 10027, United States; Department of Biological Sciences and Department of Chemistry, Columbia University, 550 West 120th Street, Northwest Corner Building, MC 4846, New York, New York 10027, United States.
Peter WipfDepartment of Chemistry, University of Pittsburgh , 219 Parkman Avenue, Pittsburgh, Pennsylvania 15260, United States.

Funding

Defining the functions and translational potential of ferroptosisR35CA209896 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI STOCKWELL, BRENT R. · 2016 to 2022
$6.5M
NCI NIH HHS R35 CA209896
6 · The paper itself

Abstract

Discovering compounds and mechanisms for inhibiting ferroptosis, a form of regulated, nonapoptotic cell death, has been of great interest in recent years. In this study, we demonstrate the ability of XJB-5-131, JP4-039, and other nitroxide-based lipid peroxidation mitigators to prevent ferroptotic cell death in HT-1080, BJeLR, and panc-1 cells. Several analogues of the reactive oxygen species (ROS) scavengers XJB-5-131 and JP4-039 were synthesized to probe structure-activity relationships and the influence of subcellular localization on the potency of these novel ferroptosis suppressors. Their biological activity correlated well over several orders of magnitude with their structure, relative lipophilicity, and respective enrichment in mitochondria, revealing a critical role of intramitochondrial lipid peroxidation in ferroptosis. These results also suggest that preventing mitochondrial lipid oxidation might offer a viable therapeutic opportunity in ischemia/reperfusion-induced tissue injury, acute kidney injury, and other pathologies that involve ferroptotic cell death pathways.

Identifiers

PMID27725964
PMCPMC5043442

What OpenQuestion holds

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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.