Evidence map›Paper›PMID 30470612›Full record

ArticleEBioMedicine2018

Evaluation of the antifibrotic potency by knocking down SPARC, CCR2 and SMAD3.

Weifeng Ding, Weilin Pu, Shuai Jiang, Yanyun Ma, Qingmei Liu, Wenyu Wu, Haiyan Chu, Hejian Zou, Li Jin, Jiucun Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. MCell death & disease · 2025
    Article
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  6. GTSE1-driven ZEB1 stabilization promotes pulmonary fibrosis through the epithelial-to-mesenchymal transition.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. The effect of human amniotic epithelial cells on urethral stricture fibroblasts.Journal of clinical and translational research · 2019
    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

11 authors at 3 institutions in 2 countries.

Weifeng DingState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China; Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China; University of Texas-McGovern Medical School, Houston, TX, USA.
Weilin PuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Shuai JiangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Yanyun MaState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Qingmei LiuDepartment of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
Wenyu WuDepartment of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
Haiyan ChuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China.
Hejian ZouDivision of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China; Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai, China.
Li JinState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China; Human Phenome Institute, Fudan University, Shanghai, China.
Jiucun WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China; Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China; Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai, China; Human Phenome Institute, Fudan University, Shanghai, China. Electronic address: jcwang@fudan.edu.cn.
Xiaodong ZhouUniversity of Texas-McGovern Medical School, Houston, TX, USA. Electronic address: xiaodong.zhou@uth.tmc.edu.
Fudan University · CNNantong University · CNThe University of Texas Health Science Center · US

Funding

Studies of HLA Region Genomics in Systemic Sclerosis and Ankylosing SpondyilitisU01AI090909 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAYES, MAUREEN MAUREEN, REVEILLE, JOHN DUFFIN · 2010 to 2014
$2.9M
NIAID NIH HHS U01 AI090909
6 · The paper itself

Abstract

backgroundThe genes of SPARC, CCR2, and SMAD3 are implicated in orchestrating inflammatory response that leads to fibrosis in scleroderma and other fibrotic disorders. The aim of the studies is to evaluate synergistic anti-fibrotic potency of the siRNAs of these genes.

methodsThe efficacy of the siRNA-combination was evaluated in bleomycin-induced mouse fibrosis. The pathological changes of skin and lungs of the mice were assessed by hematoxylin and eosin and Masson's trichrome stains. The expression of inflammation and fibrosis associated genes and proteins in the tissues were assessed by real-time RT-PCR, RNA sequencing, Western blots and ELISA. Non-crosslinked fibrillar collagen was measured by the Sircol colorimetric assay.

findingsThe applications of the combined siRNAs in bleomycin-induced mice achieved favorable anti-inflammatory and anti-fibrotic effects. Activation of fibroblasts was suppressed in parallel with inhibition of inflammation evidenced by reduced inflammatory cells and proinflammatory cytokines in the BALF and/or the tissues by the treatment. Aberrant expression of the genes normally expressed in fibroblasts, monocytes/ macrophage, endothelial and epithelial cells were significantly restrained after the treatment. In addition, transcriptome profiles indicated that some bleomycin-induced alterations of multiple biological pathways were recovered to varying degrees by the treatment.

interpretationThe application of the combined siRNAs of SPARC, CCR2, and SMAD3 genes ameliorated inflammation and fibrosis in bleomycin-induced mice. It systemically reinstated multiple biopathways, probably through controlling on different cell types including fibroblasts, monocytes/macrophages, endothelial cells and others. The multi-target-combined therapeutic approach examined herein may represent a novel and effective therapy for fibrosis.

Indexed as

AnimalsBiomarkersCytokinesDisease Models, AnimalFemaleFibrosisGene Expression ProfilingGene Knockdown TechniquesGenetic Predisposition to DiseaseInflammationInflammation MediatorsMiceOsteonectinPulmonary FibrosisReceptors, CCR2RNA InterferenceBiomarkersCcr2 protein, mouseCytokinesInflammation MediatorsOsteonectinReceptors, CCR2RNA, Small InterferingSmad3 ProteinSmad3 protein, mouseSPARC protein, mouseCCR2FibrosisInflammationMultiple targets-siRNAsPeptide nanoparticleSclerodermaSMAD3SPARC

Identifiers

PMID30470612
PMCPMC6306344
OpenAlexW2884857904

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.