Evidence map›Paper›PMID 30153328›Full record

ArticleBritish journal of pharmacology2018

Angiotensin-converting enzyme inhibitor works as a scar formation inhibitor by down-regulating Smad and TGF-β-activated kinase 1 (TAK1) pathways in mice.

Wei-Qiang Tan, Qing-Qing Fang, Xiao Z Shen, Jorge F Giani, Tuantuan V Zhao, Peng Shi, Li-Yun Zhang, Zakir Khan, You Li, Liang Li and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

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  12. Uncovering SPP1Journal of inflammation research · 2024
    Article
  13. Review
  14. Targeting the Angiotensin Pathway in the Treatment of Cutaneous Fibrosis: A Systematic Review.JID innovations : skin science from molecules to population health · 2023
    Review
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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

13 authors at 3 institutions in 2 countries.

Wei-Qiang TanDepartment of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.ORCID 0000-0003-4951-0960
Qing-Qing FangDepartment of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Xiao Z ShenDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Jorge F GianiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Tuantuan V ZhaoDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Peng ShiInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Li-Yun ZhangDepartment of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Zakir KhanDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
You LiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Liang LiDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Ji-Hua XuDepartment of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Ellen A BernsteinDepartment of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Kenneth E BernsteinDepartment of Plastic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Cedars-Sinai Medical Center · USSir Run Run Shaw Hospital · CNZhejiang International Studies University · CN

Funding

The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2016 to 2020
$12.4M
The role of angiotensin-converting enzyme in renal inflammation, kidney injury and sodium retention during diabetic nephropathyR01HL142672 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2018 to 2021
$1.7M
NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL142672
6 · The paper itself

Abstract

background and purposeAngiotensin-converting enzyme (ACE), an important part of the renin-angiotensin system, is implicated in stimulating the fibrotic processes in the heart, lung, liver and kidney, while an ACE inhibitor (ACEI) promotes physiological tissue repair in these organs. The mechanism is closely related to TGF-β1 pathways. However, the reported effects of applying ACEIs during scar formation are unclear. Hence, we explored the anti-fibrotic effects of an ACEI and the molecular mechanisms involved in a mouse scar model. EXPERIMENTAL APPROACH: After a full-thickness skin wound operation, ACE wild-type mice were randomly assigned to receive either ramipril, losartan or hydralazine p.o. ACE knockout (KO) mice and negative control mice only received vehicle (water). Wound/scar widths during wound healing and histological examinations were recorded at the final day. The ability of ACEI to reduce fibrosis via TGF-β1 signalling was evaluated in vitro and in vivo. KEY

resultsACE KO mice and mice that received ramipril showed narrower wound/scar width, reduced fibroblast proliferation, decreased collagen and TGF-β1 expression. ACEI attenuated the phosphorylation of small mothers against decapentaplegic (Smad2/3) and TGF-β-activated kinase 1 (TAK1) both in vitro and in vivo. The expression of ACE-related peptides varied in murine models with different drug treatments. CONCLUSIONS AND IMPLICATIONS: ACEI showed anti-fibrotic properties in scar formation by mediating downstream peptides to suppress TGF-β1/Smad and TGF-β1/TAK1 pathways. These findings suggest that dual inhibition of Smad and TAK1 signalling by ACEI is a useful strategy for the development of new anti-fibrotic agents.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsDisease Models, AnimalMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, KnockoutSignal TransductionSmad ProteinsAngiotensin-Converting Enzyme InhibitorsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesSmad Proteins

Identifiers

PMID30153328
PMCPMC6193878
OpenAlexW2889020113

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.