Evidence map›Paper›PMID 32975364›Full record

ArticleEMBO reports2020

Iron loss triggers mitophagy through induction of mitochondrial ferritin.

Yuichi Hara, Izumi Yanatori, Atsushi Tanaka, Fumio Kishi, John J Lemasters, Sohji Nishina, Kyo Sasaki, Keisuke Hino

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
8.7field-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

59 citing papers in PubMed, 107 citations in OpenAlex.

  1. Impact of renal iron overload on sickle cell nephropathy in a humanized mouse model.American journal of physiology. Renal physiology · 2026
    Article
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  9. Ferroptosis: biology and role in liver disease.Journal of gastroenterology · 2025
    Review
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  15. Review
  16. Article
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  18. The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Yuichi HaraDepartment of Hepatology and Pancreatology, Kawasaki Medical School, Kurashiki, Japan.
Izumi Yanatori *Department of Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.
Atsushi Tanaka *Research Institute of Medical Sciences, Yamagata University School of Medicine, Yamagata, Japan.ORCID 0000-0002-7566-2098
Fumio KishiDepartment of Molecular Genetics, Kawasaki Medical School, Kurashiki, Japan.
John J LemastersDepartment of Drug Discovery & Biomedical Sciences, Medical University of South Carolina, Charleston, SC, USA.
Sohji NishinaDepartment of Hepatology and Pancreatology, Kawasaki Medical School, Kurashiki, Japan.
Kyo SasakiDepartment of Hepatology and Pancreatology, Kawasaki Medical School, Kurashiki, Japan.
Keisuke HinoDepartment of Hepatology and Pancreatology, Kawasaki Medical School, Kurashiki, Japan.ORCID 0000-0002-3297-1720
Kawasaki Medical School · JPMedical University of South Carolina · USYamagata University · JP

Funding

Proteomics CoreP30DK123704 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DON C. ROCKEY · 2020 to 2026
$8.8M
Japan Agency for Medical Research and Development (AMED) 18fk0210016 h0003MEXT | Japan Socijety for the Promotion of Science (JSPS) 16K09384MEXT | Japan Socijety for the Promotion of Science (JSPS) 23870008MEXT | Japan Socijety for the Promotion of Science (JSPS) 26293179MEXT | Japan Socijety for the Promotion of Science (JSPS) 26870067/16K19047NIDDK NIH HHS P30 DK123704
6 · The paper itself

Abstract

Mitochondrial quality is controlled by the selective removal of damaged mitochondria through mitophagy. Mitophagy impairment is associated with aging and many pathological conditions. An iron loss induced by iron chelator triggers mitophagy by a yet unknown mechanism. This type of mitophagy may have therapeutic potential, since iron chelators are clinically used. Here, we aimed to clarify the mechanisms by which iron loss induces mitophagy. Deferiprone, an iron chelator, treatment resulted in the increased expression of mitochondrial ferritin (FTMT) and the localization of FTMT precursor on the mitochondrial outer membrane. Specific protein 1 and its regulator hypoxia-inducible factor 1α were necessary for deferiprone-induced increase in FTMT. FTMT specifically interacted with nuclear receptor coactivator 4, an autophagic cargo receptor. Deferiprone-induced mitophagy occurred selectively for depolarized mitochondria. Additionally, deferiprone suppressed the development of hepatocellular carcinoma (HCC) in mice by inducing mitophagy. Silencing FTMT abrogated deferiprone-induced mitophagy and suppression of HCC. These results demonstrate the mechanisms by which iron loss induces mitophagy and provide a rationale for targeting mitophagic activation as a therapeutic strategy.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsFerritinsIronMiceMitochondrial ProteinsMitophagyFerritinsIronMitochondrial Proteinshepatocellular carcinomairon chelatormitochondriamitochondrial ferritinmitophagy

Identifiers

PMID32975364
PMCPMC7645172
OpenAlexW3088889662

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.