Evidence map›Paper›PMID 29899565›Full record

ArticleScientific reports2018

Targeted ablation of p38α MAPK suppresses denervation-induced muscle atrophy.

Kazuki Yuasa, Kazumasa Okubo, Masaki Yoda, Kinya Otsu, Yasuyuki Ishii, Masaya Nakamura, Yoshiki Itoh, Keisuke Horiuchi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Inflammation: Roles in Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022
    Review
  19. Article
  20. 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

8 authors at 4 institutions in 2 countries.

Kazuki YuasaPharmacological R&D Section, Pharmaceutical Research Department, Sato Pharmaceutical Co., Ltd., 6-8-5 Higashi-ohi, Shinagawa, Tokyo, 140-0011, Japan.
Kazumasa OkuboPharmacological R&D Section, Pharmaceutical Research Department, Sato Pharmaceutical Co., Ltd., 6-8-5 Higashi-ohi, Shinagawa, Tokyo, 140-0011, Japan.
Masaki YodaDepartment of Orthopedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, 160-8582, Japan.
Kinya OtsuThe School of Cardiovascular Medicine and Sciences, King's College London, Strand, London, WC2R 2LS, UK.
Yasuyuki IshiiPharmacological R&D Section, Pharmaceutical Research Department, Sato Pharmaceutical Co., Ltd., 6-8-5 Higashi-ohi, Shinagawa, Tokyo, 140-0011, Japan.
Masaya NakamuraDepartment of Orthopedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, 160-8582, Japan.
Yoshiki ItohDrug Discovery Research Department, Sato Pharmaceutical Co., Ltd., 6-8-5 Higashi-ohi, Shinagawa, Tokyo, 140-0011, Japan. yoshiki.itoh@sato-seiyaku.co.jp.
Keisuke HoriuchiDepartment of Orthopedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, 160-8582, Japan. keisukehoriuchi@gmail.com.ORCID 0000-0001-7063-9609
Keio University Hospital · JPKeio University · JPKing's College London · GBWakamoto Pharmaceutical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The loss of skeletal muscle mass is a major cause of falls and fractures in the elderly, leading to compromised independence and a decrease in the quality of life. However, only a few therapeutic interventions leading to marginal clinical benefits in patients with this condition are currently available. Therefore, the demand to further understand the pathology of muscle atrophy and establish a treatment modality for patients with muscle atrophy is significant. p38α mitogen-activated protein kinase (p38α MAPK) is a ubiquitous signaling molecule that is implicated in various cellular functions, including cell proliferation, differentiation, and senescence. In the present study, we generated a mutant line in which p38α MAPK is specifically abrogated in muscle tissues. Compared with the control mice, these mutant mice are significantly resistant to denervation-induced muscle atrophy, suggesting that p38α MAPK positively regulates muscle atrophy. We also identified CAMK2B as a potential downstream target of p38α MAPK and found that the pharmacological inhibition of CAMK2B activity suppresses denervation-induced muscle atrophy. Altogether, our findings identify p38α MAPK as a novel regulator of muscle atrophy and suggest that the suppression of intracellular signaling mediated by p38α MAPK serves as a potential target for the treatment of muscle atrophy.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell LineDenervationEnzyme InhibitorsHumansMaleMice, Inbred C57BLMice, KnockoutMice, TransgenicMitogen-Activated Protein Kinase 14Molecular Targeted TherapyMuscle, SkeletalMuscular AtrophySignal TransductionCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2b protein, mouseEnzyme InhibitorsMitogen-Activated Protein Kinase 14

Identifiers

PMID29899565
PMCPMC5998077
OpenAlexW2805333204

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.