Evidence map›Paper›PMID 42618571›Full record

ArticleNature communications2026

Injury-driven stromal exhaustion disrupts intrinsic regenerative capability.

Sixun Wu, Hirotaka Matsumoto, Keita Kondo, Aiko Kuroda, Jumpei Morita, Takeshi Moriishi, Shawn A Hallett, Yuki Matsuo, Azumi Noguchi, Mitsuaki Ono and 5 more

Abstract read
In one paragraph

Article in Nature communications, 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

15 authors.

Sixun WuDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Hirotaka MatsumotoSchool of Information and Data Sciences, Nagasaki University, Nagasaki, Japan.ORCID http://orcid.org/0000-0001-9896-4817
Keita KondoDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Aiko KurodaDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Jumpei MoritaDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Takeshi MoriishiDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Shawn A HallettDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0003-1472-7502
Yuki MatsuoDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Azumi NoguchiDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Mitsuaki OnoDepartment of Oral Rehabilitation and Regenerative Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Okayama, Japan.
Makoto AbeDepartment of Tissue and Developmental Biology, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Kosei ItoDepartment of Molecular Tumor Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.ORCID http://orcid.org/0000-0002-8416-2466
Shinsuke OhbaDepartment of Tissue and Developmental Biology, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0000-0002-6874-8539
Noriaki OnoUniversity of Texas Health Science Center at Houston School of Dentistry, Houston, TX, USA.ORCID http://orcid.org/0000-0002-3771-8230
Yuki MatsushitaDepartment of Skeletal Development and Regenerative Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. yukimatsushita@nagasaki-u.ac.jp.ORCID http://orcid.org/0000-0001-9577-3249

Funding

Japan Agency for Medical Research and Development (AMED) JP256f0137009MEXT | Japan Science and Technology Agency (JST) JPMJFR2111MEXT | Japan Society for the Promotion of Science (JSPS) JP25H01073, JP24KK0168, JP21H03124, JP20KK0356
6 · The paper itself

Abstract

Bone marrow stromal cells, marked by leptin receptor (Lepr) and C-X-C motif chemokine ligand 12 (Cxcl12), orchestrate osteogenesis and maintain bone homeostasis. Following injury, these stromal cells directly generate reparative bone and subsequently restore the marrow microenvironment, a process widely regarded as a reliable regenerative response. However, it remains unclear whether stromal cells retain full regenerative capacity after prior injury. Here, we show that Lepr

Indexed as

Bone RegenerationMesenchymal Stem CellsAdipocytesAdipogenesisAnimalsbeta CateninCell DifferentiationChemokine CXCL12MiceMice, Inbred C57BLOsteogenesisReceptors, LeptinStromal CellsWnt Signaling Pathwaybeta CateninChemokine CXCL12Cxcl12 protein, mouseleptin receptor, mouseReceptors, Leptin

Identifiers

PMID42618571
PMCPMC13490406

What OpenQuestion holds

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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.