Evidence map›Paper›PMID 28942281›Full record

ArticleEBioMedicine2017

Antihypertrophic Effects of Small Molecules that Maintain Mitochondrial ATP Levels Under Hypoxia.

Hiroaki Nagai, Tomoko Satomi, Akiko Abiru, Kazumasa Miyamoto, Koji Nagasawa, Minoru Maruyama, Satoshi Yamamoto, Kuniko Kikuchi, Hiromitsu Fuse, Masakuni Noda and 1 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
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

11 authors at 1 institution in 1 country.

Hiroaki NagaiResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan. Electronic address: hiroaki.nagai@takeda.com.
Tomoko SatomiResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Akiko AbiruResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Kazumasa MiyamotoResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Koji NagasawaResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Minoru MaruyamaResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Satoshi YamamotoResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Kuniko KikuchiResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Hiromitsu FuseResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Masakuni NodaResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan.
Yoshiyuki TsujihataResearch, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa 251-8555, Japan. Electronic address: yoshiyuki.tsujihata@takeda.com.
Takeda (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since impaired mitochondrial ATP production in cardiomyocytes is thought to lead to heart failure, a drug that protects mitochondria and improves ATP production under disease conditions would be an attractive treatment option. In this study, we identified small-molecule drugs, including the anti-parasitic agent, ivermectin, that maintain mitochondrial ATP levels under hypoxia in cardiomyocytes. Mechanistically, transcriptomic analysis and gene silencing experiments revealed that ivermectin increased mitochondrial ATP production by inducing Cox6a2, a subunit of the mitochondrial respiratory chain. Furthermore, ivermectin inhibited the hypertrophic response of human induced pluripotent stem cell-derived cardiomyocytes. Pharmacological inhibition of importin β, one of the targets of ivermectin, exhibited protection against mitochondrial ATP decline and cardiomyocyte hypertrophy. These findings indicate that maintaining mitochondrial ATP under hypoxia may prevent hypertrophy and improve cardiac function, providing therapeutic options for mitochondrial dysfunction.

Indexed as

Adenosine TriphosphateAnimalsbeta KaryopherinsCardiotonic AgentsCell HypoxiaCells, CulturedElectron Transport Complex IVGene Expression ProfilingGene Expression RegulationHumansInduced Pluripotent Stem CellsIvermectinMiceMitochondriaMyocytes, CardiacSmall Molecule LibrariesAdenosine Triphosphatebeta KaryopherinsCardiotonic AgentsElectron Transport Complex IVIvermectinSmall Molecule LibrariesCardiomyocytesHypertrophyHypoxiaMitochondrial ATPPhenotypic screening

Identifiers

PMID28942281
PMCPMC5652136
OpenAlexW2755317206

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.