Evidence map›Paper›PMID 25781899›Full record

ArticlePloS one2015

Mitofusin 2-deficiency suppresses cell proliferation through disturbance of autophagy.

Yanhong Ding, Han Gao, Lifang Zhao, Xian Wang, Ming Zheng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

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  16. Redox control of vascular smooth muscle cell function and plasticity.Laboratory investigation; a journal of technical methods and pathology · 2018
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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

5 authors at 1 institution in 1 country.

Yanhong DingDepartment of Physiology and Pathophysiology, Health Science Center, Peking University, Beijing, China.
Han GaoDepartment of Physiology and Pathophysiology, Health Science Center, Peking University, Beijing, China.
Lifang ZhaoDepartment of Physiology and Pathophysiology, Health Science Center, Peking University, Beijing, China.
Xian WangDepartment of Physiology and Pathophysiology, Health Science Center, Peking University, Beijing, China.
Ming ZhengDepartment of Physiology and Pathophysiology, Health Science Center, Peking University, Beijing, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitofusin2 (Mfn2), a mitochondrial outer membrane protein serving primarily as a mitochondrial fusion protein, has multiple functions in regulating cell biological processes. Defects of Mfn2 were found in diabetes, obesity, and neurodegenerative diseases. In the present study, we found that knockdown of Mfn2 by shRNA led to impaired autophagic degradation, inhibited mitochondrial oxygen consumption rate and cell glycolysis, reduced ATP production, and suppressed cell proliferation. Inhibition of autophagic degradation mimicked Mfn2-deficiency mediated cell proliferation suppression, while enhancement of autophagosome maturation restored the suppressed cell proliferation by Mfn2-deficiency. Thus, our findings revealed the role of Mfn2 in regulating cell proliferation and mitochondrial metabolism, and shed new light on understanding the mechanisms of Mfn2 deficiency related diseases.

Indexed as

AutophagyCell ProliferationGene Knockdown TechniquesGTP PhosphohydrolasesHeLa CellsHumansMitochondriaMitochondrial ProteinsGTP PhosphohydrolasesMFN2 protein, humanMitochondrial Proteins

Identifiers

PMID25781899
PMCPMC4363693
OpenAlexW2043850619

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.