Evidence map›Paper›PMID 33438778›Full record

ReviewThe EMBO journal2021

Molecular mechanisms and physiological functions of mitophagy.

Mashun Onishi, Koji Yamano, Miyuki Sato, Noriyuki Matsuda, Koji Okamoto

Open access · hybridAbstract readReview
In one paragraph

Review in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 777 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
777citing papers in PubMed, 3 pooled it
135.4field-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

777 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,299 citations in OpenAlex.

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  16. Effects of copper overload on mitochondrial parameters in GBM-1, U-87 MG, and C6 glioma cell lines.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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717 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

5 authors at 3 institutions in 1 country.

Mashun OnishiLaboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan.ORCID 0000-0003-1511-4097
Koji YamanoThe Ubiquitin Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.ORCID 0000-0002-4692-161X
Miyuki SatoLaboratory of Molecular Membrane Biology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.ORCID 0000-0002-1944-4918
Noriyuki MatsudaThe Ubiquitin Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.ORCID 0000-0001-8199-952X
Koji OkamotoLaboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan.ORCID 0000-0003-4730-4522
The University of Osaka · JPTokyo Metropolitan Institute of Medical Science · JPGunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy-mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady-state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations.

Indexed as

Gene Regulatory NetworksAnimalsAutophagy-Related ProteinsFungiHumansMitochondriaMitochondrial ProteinsMitophagyAutophagy-Related ProteinsMitochondrial Proteinsautophagymitochondriaphosphorylationquality and quantity controlubiquitin

Identifiers

PMID33438778
PMCPMC7849173
OpenAlexW3121008513

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.