Evidence map›Paper›PMID 38891908›Full record

ArticleInternational journal of molecular sciences2024

Inflammatory Cytokine-Induced Muscle Atrophy and Weakness Can Be Ameliorated by an Inhibition of TGF-β-Activated Kinase-1.

Mai Kanai, Byambasuren Ganbaatar, Itsuro Endo, Yukiyo Ohnishi, Jumpei Teramachi, Hirofumi Tenshin, Yoshiki Higa, Masahiro Hiasa, Yukari Mitsui, Tomoyo Hara and 9 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Observational
  5. Nutrients · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
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  14. Review
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

19 authors.

Mai KanaiDepartment of Bioregulatory Sciences, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Byambasuren GanbaatarDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Itsuro EndoDepartment of Bioregulatory Sciences, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.ORCID 0000-0002-0780-0065
Yukiyo OhnishiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Jumpei TeramachiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Hirofumi TenshinDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Yoshiki HigaDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Masahiro HiasaDepartment of Orthodontics and Dentofacial Orthopedics, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.ORCID 0000-0002-4830-6274
Yukari MitsuiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Tomoyo HaraDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Shiho MasudaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Hiroki YamagamiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Yuki YamaguchiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Ken-Ichi AiharaDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Mayu SebeDepartment of Clinical Nutrition, Faculty of Health Science and Technology, Kawasaki University of Medical Welfare, Okayama 700-8570, Japan.ORCID 0009-0003-1485-5325
Rie TsutsumiDepartment of Nutrition and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.
Hiroshi SakaueDepartment of Nutrition and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.ORCID 0000-0002-2468-2363
Toshio MatsumotoFujii Memorial Institute of Medical Sciences, Tokushima University, Tokushima 770-8503, Japan.
Masahiro AbeDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan.

Funding

Grants-in-Aid for Scientific Research from the Japanese Society for Promotion of Science 21K07339
6 · The paper itself

Abstract

Chronic inflammation causes muscle wasting. Because most inflammatory cytokine signals are mediated via TGF-β-activated kinase-1 (TAK1) activation, inflammatory cytokine-induced muscle wasting may be ameliorated by the inhibition of TAK1 activity. The present study was undertaken to clarify whether TAK1 inhibition can ameliorate inflammation-induced muscle wasting. SKG/Jcl mice as an autoimmune arthritis animal model were treated with a small amount of mannan as an adjuvant to enhance the production of TNF-α and IL-1β. The increase in these inflammatory cytokines caused a reduction in muscle mass and strength along with an induction of arthritis in SKG/Jcl mice. Those changes in muscle fibers were mediated via the phosphorylation of TAK1, which activated the downstream signaling cascade via NF-κB, p38 MAPK, and ERK pathways, resulting in an increase in myostatin expression. Myostatin then reduced the expression of muscle proteins not only via a reduction in MyoD1 expression but also via an enhancement of Atrogin-1 and Murf1 expression. TAK1 inhibitor, LL-Z1640-2, prevented all the cytokine-induced changes in muscle wasting. Thus, TAK1 inhibition can be a new therapeutic target of not only joint destruction but also muscle wasting induced by inflammatory cytokines.

Indexed as

CytokinesMAP Kinase Kinase KinasesMuscular AtrophyAnimalsDisease Models, AnimalInflammationInterleukin-1betaMAP Kinase Kinase Kinase 7MiceMuscle ProteinsMuscle, SkeletalMuscle WeaknessMyostatinNF-kappa BPhosphorylationSignal TransductionCytokinesInterleukin-1betaMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMuscle ProteinsMyostatinNF-kappa BTripartite Motif ProteinsTumor Necrosis Factor-alphaZearalenoneIL-1βMyoD1myostatinTAK1 inhibitorTNF-α

Identifiers

PMID38891908
PMCPMC11172090

What OpenQuestion holds

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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.