Evidence map›Paper›PMID 30030216›Full record

ArticleEMBO reports2018

Mitochondrial hyperfusion causes neuropathy in a fly model of CMT2A.

Eri Ueda, Naotada Ishihara

Open access · bronzeAbstract readComment
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Insights Into the Role of Mitochondria in Vascular Calcification.Frontiers in cardiovascular medicine · 2022
    Review
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Eri UedaDepartment of Protein Biochemistry, Institute of Life Science, Kurume University, Kurume, Japan.
Naotada IshiharaDepartment of Protein Biochemistry, Institute of Life Science, Kurume University, Kurume, Japan.ORCID 0000-0002-6305-7149
Kurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria undergo frequent fusion and fission events, which are essential to maintain a functional mitochondrial network. A disruption of these processes can cause severe neurodegeneration. Charcot-Marie-Tooth disease type 2A (CMT2A) is a neuropathy that is caused by mutations in the fusion factor Mfn2. It is generally assumed that impaired mitochondrial fusion causes CMT2A. However, the detailed molecular mechanism underlying the pathophysiology of CMT2A is only incompletely understood. In this issue of

Indexed as

Charcot-Marie-Tooth DiseaseMitochondrial DynamicsAnimalsDrosophilaGTP PhosphohydrolasesMitochondriaMitochondrial ProteinsMutationGTP PhosphohydrolasesMitochondrial Proteins

Identifiers

PMID30030216
PMCPMC6073202
OpenAlexW2884837269

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.