Evidence map›Paper›PMID 42010905›Full record

ArticleAging cell2026

UNC45B Reduction With Aging: A Myofiber-Intrinsic Promoting Factor for Sarcopenia.

Taiga Mishima, Taiga Nagamune, Saori Tada, Daiki Watanabe, Nao Tokuda, Takashi Yamada, Akiko Hashimoto-Hachiya, Sayaka Higo-Yamamoto, Kohei Kido, Noriyuki Nagaoka and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

18 authors.

Taiga MishimaCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.
Taiga NagamuneDepartment of Life Science and Applied Chemistry, Nagoya Institute of Technology, Nagoya, Japan.
Saori TadaCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.
Daiki WatanabeGraduate School of Sport and Health Sciences, Osaka University of Health and Sport Sciences, Osaka, Japan.
Nao TokudaGraduate School of Health Sciences, Sapporo Medical University, Sapporo, Japan.
Takashi YamadaGraduate School of Health Sciences, Sapporo Medical University, Sapporo, Japan.
Akiko Hashimoto-HachiyaCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.
Sayaka Higo-YamamotoCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.
Kohei KidoHealth and Medical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Takamatsu, Japan.
Noriyuki NagaokaAdvanced Research Center for Oral and Craniofacial Sciences, Dental School, Okayama University, Okayama, Japan.
Aoi IkedoDivision of Integrative Pathophysiology, Proteo-Science Center, PIAS, Ehime University, Toon, Japan.
Yuuki ImaiDivision of Integrative Pathophysiology, Proteo-Science Center, PIAS, Ehime University, Toon, Japan.ORCID https://orcid.org/0000-0002-6119-0034
Ryo FujitaDivision of Regenerative Medicine, Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.ORCID https://orcid.org/0000-0002-8392-0122
Seiya MizunoLaboratory Animal Resource Center in Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.ORCID https://orcid.org/0000-0002-6740-5817
Satoru TakahashiLaboratory Animal Resource Center in Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.
Katsutaka OishiCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.
Satoru AtoFaculty of Medical Science, Nippon Sport Science University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0667-8790
Riki OgasawaraCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.

Funding

Japan Society for the Promotion of Science 22H03465Japan Society for the Promotion of Science 24K02820
6 · The paper itself

Abstract

Skeletal muscle mass and force decline with age, and the loss of muscle force precedes muscle atrophy. However, the underlying mechanisms remain unclear. Here, we investigated the role of the myosin co-chaperone, uncoordinated mutant number-45 myosin chaperone B (UNC45B), in regulating muscle mass and force. UNC45B expression decreased in mouse gastrocnemius muscle with age, particularly at 24 months old, and adeno-associated virus vector-mediated knockdown of Unc45b in 3-month-old mouse triceps surae muscle first reduced plantar flexor torque and then decreased gastrocnemius muscle mass. In addition, Unc45b knockdown in the triceps surae muscle resulted in lower bone mineral density. While maximum Ca

Indexed as

AgingMolecular ChaperonesMuscle Fibers, SkeletalSarcopeniaAnimalsEye MovementsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMolecular ChaperonesUnc45 protein, mousechaperonemuscle atrophymuscle forcesarcopenia

Identifiers

PMID42010905
PMCPMC13096694

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.