Evidence map›Paper›PMID 29127187›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018

Apobec2 deficiency causes mitochondrial defects and mitophagy in skeletal muscle.

Yusuke Sato, Hideaki Ohtsubo, Naohiro Nihei, Takane Kaneko, Yoriko Sato, Shin-Ichi Adachi, Shinji Kondo, Mako Nakamura, Wataru Mizunoya, Hiroshi Iida and 3 more

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Yusuke SatoDepartment of Agrobiology and Bioresources, Utsunomiya University, Tochigi, Japan.
Hideaki OhtsuboDepartment of Animal and Marine Bioresource Sciences, Kyushu University, Fukuoka, Japan.
Naohiro NiheiDepartment of Agrobiology and Bioresources, Utsunomiya University, Tochigi, Japan.
Takane KanekoDepartment of Animal and Marine Bioresource Sciences, Kyushu University, Fukuoka, Japan.
Yoriko SatoUnited Graduate School of Agricultural Science, Tokyo University of Agriculture and Technology, Tokyo, Japan.
Shin-Ichi AdachiDepartment of Agrobiology and Bioresources, Utsunomiya University, Tochigi, Japan.
Shinji KondoDepartment of Agrobiology and Bioresources, Utsunomiya University, Tochigi, Japan.
Mako NakamuraDepartment of Animal and Marine Bioresource Sciences, Kyushu University, Fukuoka, Japan.
Wataru MizunoyaDepartment of Animal and Marine Bioresource Sciences, Kyushu University, Fukuoka, Japan.
Hiroshi IidaDepartment of Animal and Marine Bioresource Sciences, Kyushu University, Fukuoka, Japan.
Ryuichi TatsumiDepartment of Animal and Marine Bioresource Sciences, Kyushu University, Fukuoka, Japan.
Cristina RadaMedical Research Council, Laboratory of Molecular Biology, Cambridge, United Kingdom.
Fumiaki YoshizawaDepartment of Agrobiology and Bioresources, Utsunomiya University, Tochigi, Japan.
Kyushu University · JPUtsunomiya University · JPMRC Laboratory of Molecular Biology · GB

Funding

Medical Research Council MC_U105178806
6 · The paper itself

Abstract

Apobec2 is a member of the activation-induced deaminase/apolipoprotein B mRNA editing enzyme catalytic polypeptide cytidine deaminase family expressed in differentiated skeletal and cardiac muscle. We previously reported that Apobec2 deficiency in mice leads to a shift in muscle fiber type, myopathy, and diminished muscle mass. However, the mechanisms of myopathy caused by Apobec2 deficiency and its physiologic functions are unclear. Here we show that, although Apobec2 localizes to the sarcomeric Z-lines in mouse tissue and cultured myotubes, the sarcomeric structure is not affected in Apobec2-deficient muscle. In contrast, electron microscopy reveals enlarged mitochondria and mitochondria engulfed by autophagic vacuoles, suggesting that Apobec2 deficiency causes mitochondrial defects leading to increased mitophagy in skeletal muscle. Indeed, Apobec2 deficiency results in increased reactive oxygen species generation and depolarized mitochondria, leading to mitophagy as a defensive response. Furthermore, the exercise capacity of Apobec2

Indexed as

AutophagyMitophagyAnimalsAPOBEC DeaminasesMiceMice, KnockoutMitochondria, MuscleMuscle ProteinsMuscle, SkeletalMuscular AtrophyReactive Oxygen SpeciesApobec2 protein, mouseAPOBEC DeaminasesMuscle ProteinsReactive Oxygen SpeciesAPOBECmitochondriamyopathy

Identifiers

PMID29127187
PMCPMC5892721
OpenAlexW2767725343

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.