Evidence map›Paper›PMID 33170806›Full record

ArticleThe Journal of clinical investigation2021

Mesenchymal Bmp3b expression maintains skeletal muscle integrity and decreases in age-related sarcopenia.

Akiyoshi Uezumi, Madoka Ikemoto-Uezumi, Heying Zhou, Tamaki Kurosawa, Yuki Yoshimoto, Masashi Nakatani, Keisuke Hitachi, Hisateru Yamaguchi, Shuji Wakatsuki, Toshiyuki Araki and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

96 citing papers in PubMed, 144 citations in OpenAlex.

  1. Loss ofiScience · 2026
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  15. Fibro-adipogenic progenitor cells from murine SMA muscles are intrinsically adipogenic.Proceedings of the National Academy of Sciences of the United States of America · 2026
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36 more citing papers are in PubMed but not listed here.

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 at 8 institutions in 1 country.

Akiyoshi UezumiMuscle Aging and Regenerative Medicine, Tokyo Metropolitan Institute of Gerontology (TMIG), Tokyo, Japan.
Madoka Ikemoto-UezumiMuscle Aging and Regenerative Medicine, Tokyo Metropolitan Institute of Gerontology (TMIG), Tokyo, Japan.
Heying ZhouMuscle Aging and Regenerative Medicine, Tokyo Metropolitan Institute of Gerontology (TMIG), Tokyo, Japan.
Tamaki KurosawaMuscle Aging and Regenerative Medicine, Tokyo Metropolitan Institute of Gerontology (TMIG), Tokyo, Japan.
Yuki YoshimotoMuscle Aging and Regenerative Medicine, Tokyo Metropolitan Institute of Gerontology (TMIG), Tokyo, Japan.
Masashi NakataniFaculty of Rehabilitation and Care, Seijoh University, Tokai, Japan.
Keisuke HitachiDivision for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan.
Hisateru YamaguchiDepartment of Medical Technology, School of Nursing and Medical Care, Yokkaichi Nursing and Medical Care University, Yokkaichi, Japan.
Shuji WakatsukiDepartment of Peripheral Nervous System Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Toshiyuki ArakiDepartment of Peripheral Nervous System Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Mitsuhiro MoritaDepartment of Orthopaedic Surgery, Fujita Health University, Toyoake, Japan.
Harumoto YamadaDepartment of Orthopaedic Surgery, Fujita Health University, Toyoake, Japan.
Masashi ToyodaVascular Medicine, TMIG, Tokyo, Japan.
Nobuo KanazawaDepartment of Surgery, Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology (TMGHIG), Tokyo, Japan.
Tatsu NakazawaSeibo Hospital, Tokyo, Japan.
Jun HinoDepartment of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan.
So-Ichiro FukadaProject for Muscle Stem Cell Biology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Kunihiro TsuchidaDivision for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan.
Tokyo Metropolitan Institute of Gerontology · JPFujita Health University · JPNational Center of Neurology and Psychiatry · JPNational Cerebral and Cardiovascular Center · JPSeijoh University · JPThe University of Osaka · JPTokyo Metropolitan Geriatric Hospital · JPYokkaichi Nursing and Medical Care University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related sarcopenia constitutes an important health problem associated with adverse outcomes. Sarcopenia is closely associated with fat infiltration in muscle, which is attributable to interstitial mesenchymal progenitors. Mesenchymal progenitors are nonmyogenic in nature but are required for homeostatic muscle maintenance. However, the underlying mechanism of mesenchymal progenitor-dependent muscle maintenance is not clear, nor is the precise role of mesenchymal progenitors in sarcopenia. Here, we show that mice genetically engineered to specifically deplete mesenchymal progenitors exhibited phenotypes markedly similar to sarcopenia, including muscle weakness, myofiber atrophy, alterations of fiber types, and denervation at neuromuscular junctions. Through searching for genes responsible for mesenchymal progenitor-dependent muscle maintenance, we found that Bmp3b is specifically expressed in mesenchymal progenitors, whereas its expression level is significantly decreased during aging or adipogenic differentiation. The functional importance of BMP3B in maintaining myofiber mass as well as muscle-nerve interaction was demonstrated using knockout mice and cultured cells treated with BMP3B. Furthermore, the administration of recombinant BMP3B in aged mice reversed their sarcopenic phenotypes. These results reveal previously unrecognized mechanisms by which the mesenchymal progenitors ensure muscle integrity and suggest that age-related changes in mesenchymal progenitors have a considerable impact on the development of sarcopenia.

Indexed as

Gene Expression RegulationAdultAgingAnimalsFemaleGrowth Differentiation Factor 10HumansMaleMesenchymal Stem CellsMiceMice, KnockoutMiddle AgedMuscle, SkeletalSarcopeniaGDF10 protein, humanGdf10 protein, mouseGrowth Differentiation Factor 10Adult stem cellsAgingMuscle BiologySkeletal muscle

Identifiers

PMID33170806
PMCPMC7773381
OpenAlexW3104428762

What OpenQuestion holds

Textmetadata
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.