Evidence map›Paper›PMID 30626897›Full record

ArticleScientific reports2019

Adiponectin promotes muscle regeneration through binding to T-cadherin.

Yoshimitsu Tanaka, Shunbun Kita, Hitoshi Nishizawa, Shiro Fukuda, Yuya Fujishima, Yoshinari Obata, Hirofumi Nagao, Shigeki Masuda, Yuto Nakamura, Yuri Shimizu and 7 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Observational
  8. T-cadherin, a major adiponectin binding partner, suppresses ERK signaling in metabolic tissues.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Ablation of UCP-1+ cells impacts FAP dynamics in muscle regeneration.American journal of physiology. Cell physiology · 2025
    Article
  17. T-Cadherin (International journal of molecular sciences · 2025
    Review
  18. Review
  19. Probiotics and muscle health: the impact ofFrontiers in microbiology · 2025
    Review
  20. Article

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 2 countries.

Yoshimitsu TanakaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shunbun KitaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan. shunkita@endmet.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0002-8937-0053
Hitoshi NishizawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shiro FukudaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yuya FujishimaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yoshinari ObataDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Hirofumi NagaoDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shigeki MasudaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yuto NakamuraDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yuri ShimizuDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Ryohei MineoDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tomoaki NatsukawaDepartment of emergency & intensive care, Yodogawa Christian Hospital, Osaka, Japan.
Tohru FunahashiDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Barbara RanschtSanford Burnham Prebys Medical Discovery Institute, NIH-designated Cancer Center, Development, Aging and Regeneration Program, La Jolla, CA, USA.
So-Ichiro FukadaLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.ORCID http://orcid.org/0000-0003-4051-5108
Norikazu MaedaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Iichiro ShimomuraDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
The University of Osaka · JPOsaka City University · JPSanford Burnham Prebys Medical Discovery Institute · USYodogawa Christian Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle has remarkable regenerative potential and its decline with aging is suggested to be one of the important causes of loss of muscle mass and quality of life in elderly adults. Metabolic abnormalities such as obesity were linked with decline of muscle regeneration. On the other hand, plasma levels of adiponectin are decreased in such metabolic conditions. However, plasma levels of adiponectin have been shown to inversely correlate with muscle mass and strength in elderly people especially with chronic heart failure (CHF). Here we have addressed whether adiponectin has some impact on muscle regeneration after cardiotoxin-induced muscle injury in mice. Muscle regeneration was delayed by angiotensin II infusion, mimicking aging and CHF as reported. Adiponectin overexpression in vivo decreased necrotic region and increased regenerating myofibers. Such enhanced regeneration by excess adiponectin was also observed in adiponectin null mice, but not in T-cadherin null mice. Mechanistically, adiponectin accumulated on plasma membrane of myofibers both in mice and human, and intracellularly colocalized with endosomes positive for a multivesicular bodies/exosomes marker CD63 in regenerating myofibers. Purified high-molecular multimeric adiponectin similarly accumulated intracellularly and colocalized with CD63-positive endosomes and enhanced exosome secretion in differentiating C2C12 myotubes but not in undifferentiated myoblasts. Knockdown of T-cadherin in differentiating C2C12 myotubes attenuated both adiponectin-accumulation and adiponectin-mediated exosome production. Collectively, our studies have firstly demonstrated that adiponectin stimulates muscle regeneration through T-cadherin, where intracellular accumulation and exosome-mediated process of adiponectin may have some roles.

Indexed as

Muscle, SkeletalRegenerationAdiponectinAgingAnimalsCadherinsCell LineHeart FailureHumansMiceMice, Inbred C57BLAdiponectinADIPOQ protein, humanAdipoq protein, mouseCadherinsH-cadherin

Identifiers

PMID30626897
PMCPMC6327035
OpenAlexW2910728038

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.