Evidence map›Paper›PMID 37019910›Full record

ArticleNPJ Regenerative medicine2023

Odd skipped-related 1 controls the pro-regenerative response of fibro-adipogenic progenitors.

Georgios Kotsaris, Taimoor H Qazi, Christian H Bucher, Hafsa Zahid, Sophie Pöhle-Kronawitter, Vladimir Ugorets, William Jarassier, Stefan Börno, Bernd Timmermann, Claudia Giesecke-Thiel and 6 more

Abstract read
In one paragraph

Article in NPJ Regenerative medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Review
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  11. Vascular adhesion molecule 1JVS-vascular science · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Thrown for a loop: fibro-adipogenic progenitors in skeletal muscle fibrosis.American journal of physiology. Cell physiology · 2023
    Review
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

16 authors.

Georgios KotsarisInstitute of Chemistry and Biochemistry, Musculoskeletal Development and Regeneration Group, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany.ORCID http://orcid.org/0000-0002-8661-7671
Taimoor H Qazi *Berlin Institute of Health at Charité - Universitätsmedizin Berlin, BIH Julius Wolff Institute, Augustenburger Platz 1, 13353, Berlin, Germany.
Christian H Bucher *Berlin Institute of Health at Charité - Universitätsmedizin Berlin, BIH Julius Wolff Institute, Augustenburger Platz 1, 13353, Berlin, Germany.ORCID http://orcid.org/0000-0002-3900-088X
Hafsa ZahidInstitute of Chemistry and Biochemistry, Musculoskeletal Development and Regeneration Group, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany.
Sophie Pöhle-KronawitterInstitute of Chemistry and Biochemistry, Musculoskeletal Development and Regeneration Group, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany.ORCID http://orcid.org/0000-0003-4874-6971
Vladimir UgoretsInstitute of Chemistry and Biochemistry, Cell Signaling Group, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany.
William JarassierInstitut NeuroMyoGène, CNRS UMR 5261, Inserm U1315, Université Claude Bernard Lyon 1, 69008, Lyon, France.
Stefan BörnoMax Planck Institute for Molecular Genetics, Ihnestrasse 73, 14195, Berlin, Germany.
Bernd TimmermannMax Planck Institute for Molecular Genetics, Ihnestrasse 73, 14195, Berlin, Germany.
Claudia Giesecke-ThielMax Planck Institute for Molecular Genetics, Ihnestrasse 73, 14195, Berlin, Germany.ORCID http://orcid.org/0000-0002-5927-7018
Aris N EconomidesRegeneron Pharmaceuticals Inc., Tarrytown, NY, USA.ORCID http://orcid.org/0000-0002-6508-8942
Fabien Le GrandInstitut NeuroMyoGène, CNRS UMR 5261, Inserm U1315, Université Claude Bernard Lyon 1, 69008, Lyon, France.ORCID http://orcid.org/0000-0002-7843-3899
Pedro Vallecillo-GarcíaInstitute of Chemistry and Biochemistry, Musculoskeletal Development and Regeneration Group, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany.
Petra KnausBerlin-Brandenburg School for Regenerative Therapies, Charité - Universitätsmedizin Berlin, 13353, Berlin, Germany.ORCID http://orcid.org/0000-0003-2492-1667
Sven GeisslerBerlin Institute of Health at Charité - Universitätsmedizin Berlin, BIH Julius Wolff Institute, Augustenburger Platz 1, 13353, Berlin, Germany.ORCID http://orcid.org/0000-0002-8750-6324
Sigmar StrickerInstitute of Chemistry and Biochemistry, Musculoskeletal Development and Regeneration Group, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany. sigmar.stricker@fu-berlin.de.ORCID http://orcid.org/0000-0002-7174-5363

Funding

Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research) 031L0234BDeutsche Forschungsgemeinschaft (German Research Foundation) CRC 1444Deutsche Forschungsgemeinschaft (German Research Foundation) GE2512/2-2EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 779293
6 · The paper itself

Abstract

Skeletal muscle regeneration requires the coordinated interplay of diverse tissue-resident- and infiltrating cells. Fibro-adipogenic progenitors (FAPs) are an interstitial cell population that provides a beneficial microenvironment for muscle stem cells (MuSCs) during muscle regeneration. Here we show that the transcription factor Osr1 is essential for FAPs to communicate with MuSCs and infiltrating macrophages, thus coordinating muscle regeneration. Conditional inactivation of Osr1 impaired muscle regeneration with reduced myofiber growth and formation of excessive fibrotic tissue with reduced stiffness. Osr1-deficient FAPs acquired a fibrogenic identity with altered matrix secretion and cytokine expression resulting in impaired MuSC viability, expansion and differentiation. Immune cell profiling suggested a novel role for Osr1-FAPs in macrophage polarization. In vitro analysis suggested that increased TGFβ signaling and altered matrix deposition by Osr1-deficient FAPs actively suppressed regenerative myogenesis. In conclusion, we show that Osr1 is central to FAP function orchestrating key regenerative events such as inflammation, matrix secretion and myogenesis.

Identifiers

PMID37019910
PMCPMC10076435

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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.