Evidence map›Paper›PMID 27901027›Full record

ArticleScientific reports2016

Targeted killing of myofibroblasts by biosurfactant di-rhamnolipid suggests a therapy against scar formation.

Chong Shen, Lifang Jiang, Huawei Shao, Chuangang You, Guoliang Zhang, Sitong Ding, Tingwei Bian, Chunmao Han, Qin Meng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 45 citations in OpenAlex.

  1. Dirhamnolipids fromACS omega · 2026
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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

9 authors at 3 institutions in 1 country.

Chong ShenCollege of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.
Lifang JiangCollege of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.
Huawei ShaoDepartment of Burns &Wound Care Centre, Second Affiliated Hospital of Zhejiang University, College of Medicine, Hangzhou, PR China.
Chuangang YouDepartment of Burns &Wound Care Centre, Second Affiliated Hospital of Zhejiang University, College of Medicine, Hangzhou, PR China.
Guoliang ZhangOcean College, Zhejiang University of Technology, Hangzhou, PR China.
Sitong DingCollege of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.
Tingwei BianCollege of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.
Chunmao HanDepartment of Burns &Wound Care Centre, Second Affiliated Hospital of Zhejiang University, College of Medicine, Hangzhou, PR China.
Qin MengCollege of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.
Zhejiang University · CNSecond Affiliated Hospital of Zhejiang University · CNZhejiang University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathological myofibroblasts are often involved in skin scarring via generating contractile force and over-expressing collagen fibers, but no compound has been found to inhibit the myofibroblasts without showing severe toxicity to surrounding physiological cells. Here we report that di-rhamnolipid, a biosurfactant secreted by Pseudomonas aeruginosa, showed potent effects on scar therapy via a unique mechanism of targeted killing the myofibroblasts. In cell culture, the fibroblasts-derived myofibroblasts were more sensitive to di-rhamnolipid toxicity than fibroblasts at a concentration-dependent manner, and could be completely inhibited of their specific functions including α-SMA expression and collagen secretion/contraction. The anti-fibrotic function of di-rhamnolipid was further verified in rabbit ear hypertrophic scar models by presenting the significant reduction of scar elevation index, type I collagen fibers and α-SMA expression. In this regard, di-rhamnolipid treatment could be suggested as a therapy against skin scarring.

Indexed as

ActinsAnimalsCell DifferentiationCicatrix, HypertrophicCollagen Type IEarFibroblastsGene ExpressionGlycolipidsMaleMolecular Targeted TherapyMyofibroblastsPseudomonas aeruginosaRabbitsSkinSurface-Active AgentsActinsCollagen Type IGlycolipidsrhamnolipid hemolysin, Pseudomonas aeruginosaSurface-Active Agents

Identifiers

PMID27901027
PMCPMC5128858
OpenAlexW2558315648

What OpenQuestion holds

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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.