Evidence map›Paper›PMID 42316943›Full record

ArticleJournal of cachexia, sarcopenia and muscle2026

Deletion of Tgf-β1 From CD206

Muhammad Bilal, Le Duc Anh, Nguyen Quynh Phuong, Sana Khalid, Allah Nawaz, Memoona, Muhammad Rahil Aslam, Tomonobu Kado, Yoshiyuki Watanabe, Ayumi Nishimura and 13 more

Abstract read
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In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

23 authors.

Muhammad BilalFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Le Duc AnhFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Nguyen Quynh PhuongFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Sana KhalidDepartment of Molecular Neuroscience, Faculty of Medicine, University of Toyama, Toyama, Japan.
Allah NawazSection of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA.
MemoonaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Muhammad Rahil AslamFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Tomonobu KadoFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Yoshiyuki WatanabeFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Ayumi NishimuraFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Yoshiko IgarashiFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Aamir SharifDepartment of Neurophysiology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
Yasuhiro OnogiResearch Center for Pre-Disease Science, Faculty of Education and Research Promotion, University of Toyama, Toyama, Japan.
Tsutomu WadaDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Ryuji HayashiClinical Oncology, Faculty of Medicine, University of Toyama, Toyama, Japan.
Kenichi HirabayashiDepartment of Diagnostic Pathology, Faculty of Medicine, University of Toyama, Toyama, Japan.
Seiji YamamotoDepartment of Pathology, Faculty of Medicine, University of Toyama, Toyama, Japan.
Takashi NakagawaDepartment of Molecular and Medical Pharmacology, Faculty of Medicine, University of Toyama, Toyama, Japan.
Hisashi MoriDepartment of Molecular Neuroscience, Faculty of Medicine, University of Toyama, Toyama, Japan.
Isao UsuiDepartment of Endocrinology and Metabolism, Dokkyo Medical University, Tochigi, Japan.
Masaru KatoFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Shiho FujisakaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan.
Kazuyuki TobeResearch Center for Pre-Disease Science, Faculty of Education and Research Promotion, University of Toyama, Toyama, Japan.ORCID https://orcid.org/0000-0003-0015-0255

Funding

Boehringer IngelheimEli Lilly Japan KK Innovation Research GrantFirst Bank of Toyama Scholarship FoundationHokugin Young Researchers GrantJapan Association for Diabetes Education and CareJapan Diabetes FoundationJapan Diabetes SocietyJapan Foundation for Applied EnzymologyJapan Society for the Promotion of Science 21K16338Japan Society for the Promotion of Science 22K16423Japan Society for the Promotion of Science 22K16424Japan Society for the Promotion of Science 22K203737Japan Society for the Promotion of Science 23KJ1022Japan Society for the Promotion of Science 24K02502Japan Society for the Promotion of Science 24K19282Japan Society for the Promotion of Science 24K19303Japan Society for the Study of ObesityLotte FoundationMoonshot R&D JPMJMS2021Naito FoundationNovo Nordisk PharmaONO Medical Research FoundationSuzuken Memorial FoundationUehara Memorial Foundation 2023Yamaguchi Endocrine Research Foundation
6 · The paper itself

Abstract

backgroundsObesity and diabetes impair the ability of the muscle to regenerate, repair and remodel, resulting in a gradual decrease in muscle mass and function. However, the underlying mechanisms and effective therapeutic strategies remain poorly understood. M2 macrophages within skeletal muscle play an important role in tissue recovery following injury. This study aims to investigate the role of M2 macrophages derived transforming growth factor-beta 1 (Tgf-β1) in regulation of skeletal muscle function under diet-induced obese conditions.

methodsAn CD206

resultsThe present findings demonstrated improved exercise performance, as evidenced by increased running distance twice (p = 0.0008) in Tgf-β1 KO mice. Deletion of CD206

conclusionsThe CD206

Indexed as

AMP-Activated Protein KinasesLectins, C-TypeMacrophagesMannose-Binding LectinsMuscle DevelopmentMuscle, SkeletalObesityReceptors, Cell SurfaceTransforming Growth Factor beta1AnimalsDiet, High-FatGene DeletionMaleMannose ReceptorMiceMice, KnockoutAMP-Activated Protein KinasesLectins, C-TypeMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceTransforming Growth Factor beta1M2 macrophage‐derived Tgf‐β1mitochondrial functionmuscle dysfunctionsarcopenic obesity

Identifiers

PMID42316943
PMCPMC13280218

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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.