Evidence map›Paper›PMID 31740582›Full record

ArticleThe Journal of biological chemistry2020

Ferroptosis is controlled by the coordinated transcriptional regulation of glutathione and labile iron metabolism by the transcription factor BACH1.

Hironari Nishizawa, Mitsuyo Matsumoto, Tomohiko Shindo, Daisuke Saigusa, Hiroki Kato, Katsushi Suzuki, Masaki Sato, Yusho Ishii, Hiroaki Shimokawa, Kazuhiko Igarashi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

160 citing papers in PubMed, 269 citations in OpenAlex.

  1. Review
  2. Review
  3. Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026
    Review
  4. Article
  5. Review
  6. Review
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  9. ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  19. Article
  20. Association ofBiomedicines · 2025
    Article

100 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

10 authors at 1 institution in 1 country.

Hironari NishizawaDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Mitsuyo MatsumotoDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan; Center for Regulatory Epigenome and Diseases, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Tomohiko ShindoDepartment of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Daisuke SaigusaDepartment of Integrative Genomics, Tohoku University Tohoku Medical Megabank Organization, Seiryo-machi 2-1, Sendai 980-8573, Japan.
Hiroki KatoDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Katsushi SuzukiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Masaki SatoDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Yusho IshiiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Hiroaki ShimokawaDepartment of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan.
Kazuhiko IgarashiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan; Center for Regulatory Epigenome and Diseases, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Sendai 980-8575, Japan. Electronic address: igarashi@med.tohoku.ac.jp.
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is an iron-dependent programmed cell death event, whose regulation and physiological significance remain to be elucidated. Analyzing transcriptional responses of mouse embryonic fibroblasts exposed to the ferroptosis inducer erastin, here we found that a set of genes related to oxidative stress protection is induced upon ferroptosis. We considered that up-regulation of these genes attenuates ferroptosis induction and found that the transcription factor BTB domain and CNC homolog 1 (BACH1), a regulator in heme and iron metabolism, promotes ferroptosis by repressing the transcription of a subset of the erastin-induced protective genes. We noted that these genes are involved in the synthesis of GSH or metabolism of intracellular labile iron and include

Indexed as

FerroptosisAmino Acid Transport System y+AnimalsBasic-Leucine Zipper Transcription FactorsCation Transport ProteinsCells, CulturedFerritinsFerroportinFibroblastsGlutamate-Cysteine LigaseGlutathioneIronMiceMice, Inbred C57BLMyocardial InfarctionMyocytes, CardiacAmino Acid Transport System y+Bach1 protein, mouseBasic-Leucine Zipper Transcription FactorsCation Transport ProteinsFerritinsFerroportinFth1 protein, mouseGCLM protein, mouseGlutamate-Cysteine LigaseGlutathioneIronOxidoreductasesSlc7a11 protein, mouse(BTB domain and CNC homolog 1) BACH1cardiovascular diseasecell deathferroptosisglutathione peroxidaseironiron sequestrationischemiamyocardial infarctiontranscription repressor

Identifiers

PMID31740582
PMCPMC6952604
OpenAlexW2990511618

What OpenQuestion holds

Textmetadata
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.