Evidence map›Paper›PMID 32183151›Full record

ArticleCells2020

The Transcription Factor Nfix Requires RhoA-ROCK1 Dependent Phagocytosis to Mediate Macrophage Skewing during Skeletal Muscle Regeneration.

Marielle Saclier, Michela Lapi, Chiara Bonfanti, Giuliana Rossi, Stefania Antonini, Graziella Messina

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.8field-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

35 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Dynamic NFIX Promoter Usage Shapes Stem and Committed Myogenic States.International journal of molecular sciences · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. [Nuclear Factor I-X Regulates Molecular Pathways Related to Craniofacial Development Through Phase Separation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. NFIXing Cancer: The Role of NFIX in Oxidative Stress Response and Cell Fate.International journal of molecular sciences · 2023
    Review
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Marielle SaclierDepartment of Biosciences, University of Milan, via Celoria 26, 20133, Milan, Italy.
Michela LapiDepartment of Biosciences, University of Milan, via Celoria 26, 20133, Milan, Italy.
Chiara BonfantiDepartment of Biosciences, University of Milan, via Celoria 26, 20133, Milan, Italy.
Giuliana RossiDepartment of Biosciences, University of Milan, via Celoria 26, 20133, Milan, Italy.
Stefania AntoniniDepartment of Biosciences, University of Milan, via Celoria 26, 20133, Milan, Italy.
Graziella MessinaDepartment of Biosciences, University of Milan, via Celoria 26, 20133, Milan, Italy.
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages (MPs) are immune cells which are crucial for tissue repair. In skeletal muscle regeneration, pro-inflammatory cells first infiltrate to promote myogenic cell proliferation, then they switch into an anti-inflammatory phenotype to sustain myogenic cells differentiation and myofiber formation. This phenotypical switch is induced by dead cell phagocytosis. We previously demonstrated that the transcription factor Nfix, a member of the nuclear factor I (Nfi) family, plays a pivotal role during muscle development, regeneration and in the progression of muscular dystrophies. Here, we show that Nfix is mainly expressed by anti-inflammatory macrophages. Upon acute injury, mice deleted for Nfix in myeloid line displayed a significant defect in the process of muscle regeneration. Indeed, Nfix is involved in the macrophage phenotypical switch and macrophages lacking Nfix failed to adopt an anti-inflammatory phenotype and interact with myogenic cells. Moreover, we demonstrated that phagocytosis induced by the inhibition of the RhoA-ROCK1 pathway leads to Nfix expression and, consequently, to acquisition of the anti-inflammatory phenotype. Our study identified Nfix as a link between RhoA-ROCK1-dependent phagocytosis and the MP phenotypical switch, thus establishing a new role for Nfix in macrophage biology for the resolution of inflammation and tissue repair.

Indexed as

RegenerationAnimalsCell DifferentiationCell ProliferationInflammationMacrophagesMiceMice, KnockoutMuscle, SkeletalMyoblasts, SkeletalNFI Transcription FactorsPhagocytosisrhoA GTP-Binding Proteinrho-Associated KinasesNFI Transcription FactorsNfix protein, mouserhoA GTP-Binding ProteinRhoA protein, mouserho-Associated KinasesRock1 protein, mousemacrophagesNfixphagocytosisRhoA-ROCK1skeletal muscle

Identifiers

PMID32183151
PMCPMC7140652
OpenAlexW3011097299

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.