Evidence map›Paper›PMID 23103763›Full record

ArticleThe EMBO journal2012

Reciprocal expression of MRTF-A and myocardin is crucial for pathological vascular remodelling in mice.

Takeya Minami, Koichiro Kuwahara, Yasuaki Nakagawa, Minoru Takaoka, Hideyuki Kinoshita, Kazuhiro Nakao, Yoshihiro Kuwabara, Yuko Yamada, Chinatsu Yamada, Junko Shibata and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

60 citing papers in PubMed, 100 citations in OpenAlex.

  1. Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026
    Review
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  3. Article
  4. Review
  5. Article
  6. Review
  7. Engineering a serum response factor superactivator of smooth muscle gene expression with a condensate-forming domain.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Circulation · 2023
    Article
  15. Rho/SRF Inhibitor Modulates Mitochondrial Functions.International journal of molecular sciences · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

22 authors at 7 institutions in 2 countries.

Takeya MinamiDepartment of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Koichiro Kuwahara
Yasuaki Nakagawa
Minoru Takaoka
Hideyuki Kinoshita
Kazuhiro Nakao
Yoshihiro Kuwabara
Yuko Yamada
Chinatsu Yamada
Junko Shibata
Satoru Usami
Shinji Yasuno
Toshio Nishikimi
Kenji Ueshima
Masataka Sata
Hiroyasu Nakano
Takahiro Seno
Yutaka Kawahito
Kenji Sobue
Akinori Kimura
Ryozo Nagai
Kazuwa Nakao
Kyoto University · JPKyoto Prefectural University of Medicine · JPThe University of Tokyo · JPBiochemical Society · GBIwate Medical University · JPTokushima University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardin-related transcription factor (MRTF)-A is a Rho signalling-responsive co-activator of serum response factor (SRF). Here, we show that induction of MRTF-A expression is key to pathological vascular remodelling. MRTF-A expression was significantly higher in the wire-injured femoral arteries of wild-type mice and in the atherosclerotic aortic tissues of ApoE(-/-) mice than in healthy control tissues, whereas myocardin expression was significantly lower. Both neointima formation in wire-injured femoral arteries in MRTF-A knockout (Mkl1(-/-)) mice and atherosclerotic lesions in Mkl1(-/-); ApoE(-/-) mice were significantly attenuated. Expression of vinculin, matrix metallopeptidase 9 (MMP-9) and integrin β1, three SRF targets and key regulators of cell migration, in injured arteries was significantly weaker in Mkl1(-/-) mice than in wild-type mice. In cultured vascular smooth muscle cells (VSMCs), knocking down MRTF-A reduced expression of these genes and significantly impaired cell migration. Underlying the increased MRTF-A expression in dedifferentiated VSMCs was the downregulation of microRNA-1. Moreover, the MRTF-A inhibitor CCG1423 significantly reduced neointima formation following wire injury in mice. MRTF-A could thus be a novel therapeutic target for the treatment of vascular diseases.

Indexed as

AnimalsAtherosclerosisCell MovementCells, CulturedChlorocebus aethiopsCOS CellsFemoral ArteryImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMuscle, Smooth, VascularMyocardinNeointimaNIH 3T3 CellsMrtfa protein, mouseMyocardinNuclear ProteinsSerum Response FactorTrans-Activators

Identifiers

PMID23103763
PMCPMC3512386
OpenAlexW2149258710

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.