Evidence map›Paper›PMID 31061094›Full record

ArticleMolecular and cellular biology2019

Iron Supply via NCOA4-Mediated Ferritin Degradation Maintains Mitochondrial Functions.

Motoki Fujimaki, Norihiko Furuya, Shinji Saiki, Taku Amo, Yoko Imamichi, Nobutaka Hattori

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

  1. Pharmaceutical biology · 2026
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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

6 authors at 2 institutions in 1 country.

Motoki FujimakiDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Norihiko FuruyaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan nohuruya@juntendo.ac.jp nhattori@juntendo.ac.jp.ORCID 0000-0001-7695-4271
Shinji SaikiDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Taku AmoDepartment of Applied Chemistry, National Defense Academy, Yokosuka, Kanagawa, Japan.
Yoko ImamichiDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan nohuruya@juntendo.ac.jp nhattori@juntendo.ac.jp.
Juntendo University · JPNational Defense Academy of Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron is an essential nutrient for mitochondrial metabolic processes, including mitochondrial respiration. Ferritin complexes store excess iron and protect cells from iron toxicity. Therefore, iron stored in the ferritin complex might be utilized under iron-depleted conditions. In this study, we show that the inhibition of lysosome-dependent protein degradation by bafilomycin A1 and the knockdown of NCOA4, an autophagic receptor for ferritin, reduced mitochondrial respiration, respiratory chain complex assembly, and membrane potential under iron-sufficient conditions. However, autophagy did not contribute to degradation of the ferritin complex under iron-sufficient conditions. Knockout of the ferritin light chain, a subunit of the ferritin complex, inhibited ferritin degradation by decreasing interactions with NCOA4. However, ferritin light chain knockout did not affect mitochondrial functions under iron-sufficient conditions, and ferritin light chain knockout cells showed a rapid reduction of mitochondrial functions compared with wild-type cells under iron-depleted conditions. These results indicate that the constitutive degradation of the ferritin complex contributes to the maintenance of mitochondrial functions.

Indexed as

AutophagyCell RespirationFerritinsGene Knockdown TechniquesHeLa CellsHumansIronLysosomesMacrolidesMembrane Potential, MitochondrialMitochondriaNuclear Receptor CoactivatorsProteolysisbafilomycin A1FerritinsIronMacrolidesNCOA4 protein, humanNuclear Receptor Coactivatorsferritin complexferritin heavy chainferritin light chainironlysosomemitochondriamitochondrial respirationmitochondrial respiratory chain complexNCOA4

Identifiers

PMID31061094
PMCPMC6597882
OpenAlexW2943244321

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.