Evidence map›Paper›PMID 39384404›Full record

ArticleAging cell2024

Cellular senescence by loss of Men1 in osteoblasts is critical for age-related osteoporosis.

Yuichiro Ukon, Takashi Kaito, Hiromasa Hirai, Takayuki Kitahara, Masayuki Bun, Joe Kodama, Daisuke Tateiwa, Shinichi Nakagawa, Masato Ikuta, Takuya Furuichi and 8 more

Abstract read
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
  2. Article
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  5. Article
  6. Review
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  8. Article
  9. Review
  10. Biomaterials science · 2025
    Review
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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.

Yuichiro UkonDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.ORCID 0000-0002-0747-8854
Takashi KaitoDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Hiromasa HiraiDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Takayuki KitaharaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Masayuki BunDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Joe KodamaDepartment of Orthopedics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Daisuke TateiwaDepartment of Orthopaedic Surgery, Osaka General Medical Center, Osaka, Osaka, Japan.
Shinichi NakagawaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Masato IkutaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Takuya FuruichiDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yuya KanieDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Takahito FujimoriDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Shota TakenakaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Tadashi YamamuroDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-0610-5204
Satoru OtsuruDepartment of Orthopedics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Seiji OkadaDepartment of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Masakatsu YamashitaDepartment of Immunology, Ehime University Graduate School of Medicine, Toon, Ehime, Japan.
Takeshi ImamuraDepartment of Molecular Medicine for Pathogenesis, Ehime University Graduate School of Medicine, Toon, Ehime, Japan.

Funding

Asahi Kasei Joint Research FoundationJapan Society for the Promotion of Science 20K09479Japan Society for the Promotion of Science 22K20960Japan Society for the Promotion of Science 23K15689
6 · The paper itself

Abstract

Recent evidence suggests an association between age-related osteoporosis and cellular senescence in the bone; however, the specific bone cells that play a critical role in age-related osteoporosis and the mechanism remain unknown. Results revealed that age-related osteoporosis is characterized by the loss of osteoblast Men1. Osteoblast-specific inducible knockout of Men1 caused structural changes in the mice bones, matching the phenotypes in patients with age-related osteoporosis. Histomorphometrically, Men1-knockout mice femurs decreased osteoblastic activity and increased osteoclastic activity, hallmarks of age-related osteoporosis. Loss of Men1 induces cellular senescence via mTORC1 activation and AMPK suppression, rescued by metformin treatment. In bone morphogenetic protein-indued bone model, loss of Men1 leads to accumulation of senescent cells and osteoporotic bone formation, which are ameliorated by metformin. Our results indicate that cellular senescence in osteoblasts plays a critical role in age-related osteoporosis and that osteoblast-specific inducible Men1-knockout mice offer a promising model for developing therapeutics for age-related osteoporosis.

Indexed as

Cellular SenescenceOsteoblastsOsteoporosisProto-Oncogene ProteinsAgingAnimalsHumansMetforminMiceMice, KnockoutMen1 protein, mouseMetforminProto-Oncogene ProteinsAMPKcellular senescenceMen1mTORC1osteoporosis

Identifiers

PMID39384404
PMCPMC11464108

What Socratic 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 Socratic graph.