Evidence map›Paper›PMID 27777101›Full record

ArticleThe Journal of investigative dermatology2017

Glycyrrhizin Ameliorates Fibrosis, Vasculopathy, and Inflammation in Animal Models of Systemic Sclerosis.

Takashi Yamashita, Yoshihide Asano, Takashi Taniguchi, Kouki Nakamura, Ryosuke Saigusa, Shunsuke Miura, Tetsuo Toyama, Takehiro Takahashi, Yohei Ichimura, Ayumi Yoshizaki and 2 more

Abstract read
In one paragraph

Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021
    Review
  17. Review
  18. Article
  19. Article
  20. Emerging Roles of Matricellular Proteins in Systemic Sclerosis.International journal of molecular sciences · 2020
    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

12 authors at 2 institutions in 2 countries.

Takashi YamashitaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Yoshihide AsanoDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan. Electronic address: yasano-tky@umin.ac.jp.
Takashi TaniguchiDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Kouki NakamuraDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Ryosuke SaigusaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Shunsuke MiuraDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Tetsuo ToyamaDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Takehiro TakahashiDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Yohei IchimuraDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Ayumi YoshizakiDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Maria TrojanowskaArthritis Center, Boston University School of Medicine, Boston, Massachusetts, USA.
Shinichi SatoDepartment of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
The University of Tokyo · JPBoston University · US

Funding

Translational studies for identifying and targeting novel pathways in systemic sclerosis pathogenesisP50AR060780 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAFYATIS, ROBERT A. · 2011 to 2021
$14.9M
The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
TGF BETA RECEPTOR SIGNALING IN SCLERODERMAR01AR044883 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2012
$3.3M
NIAMS NIH HHS P50 AR060780NIAMS NIH HHS R01 AR042334NIAMS NIH HHS R01 AR044883
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a multisystem inflammatory and vascular disease resulting in extensive tissue fibrosis. Glycyrrhizin, clinically used for chronic hepatic diseases and itching dermatitis, modulates the pathological processes of inflammation, vasculopathy, and fibrosis in human diseases and their animal models. Therefore, we investigated a potential impact of glycyrrhizin on the key pathological manifestations of SSc, including inflammation, vasculopathy, and tissue fibrosis, with bleomycin-treated mice mimicking the fibrotic and inflammatory components of SSc and endothelial cell-specific Fli1-knockout mice recapitulating SSc vasculopathy. Glycyrrhizin significantly ameliorated dermal fibrosis in bleomycin-treated mice, which was partly attributable to blockade of transforming growth factor-β signaling in dermal fibroblasts through the down-regulation of thrombospondin 1, a latent transforming growth factor-β receptor, and transcription factors Smad3 and Ets1. Furthermore, bleomycin-dependent induction of T helper type 2-skewed immune polarization, M2 macrophage infiltration, and endothelial-to-mesenchymal transition were greatly suppressed in mice administered glycyrrhizin. Glycyrrhizin also improved vascular permeability of endothelial cell-specific Fli1-knockout mice by increasing the expression of molecules regulating vascular integrity. These results indicate that glycyrrhizin ameliorates bleomycin-induced dermal fibrosis through the inhibition of fibroblast activation, T helper type 2-skewed immune polarization, M2 macrophage infiltration, and endothelial-to-mesenchymal transition and improves endothelial Fli1 deficiency-dependent vascular disintegrity, implying its potential as a disease-modifying drug for SSc.

Indexed as

AnimalsBleomycinDisease Models, AnimalFibroblastsFibrosisGlycyrrhizic AcidHumansInflammationMiceMice, Inbred C57BLMice, KnockoutPhenotypeScleroderma, SystemicSkinTh2 CellsTransforming Growth Factor betaBleomycinGlycyrrhizic AcidTransforming Growth Factor beta

Identifiers

PMID27777101
PMCPMC5380226
OpenAlexW2532708064

What OpenQuestion holds

Textmetadata
LicenceTDM
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.