Evidence map›Paper›PMID 31217321›Full record

ReviewClinical science (London, England : 1979)2019

Application of nintedanib and other potential anti-fibrotic agents in fibrotic diseases.

Feng Liu, George Bayliss, Shougang Zhuang

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Peptide Angio-3 Attenuates Pulmonary Fibrosis Via Modulation of the Coagulation Factor Xa-Protease-Activated Receptor-1 Signaling Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
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  5. [Research progress on cellular metabolic reprogramming in skin fibrosis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    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

3 authors at 2 institutions in 2 countries.

Feng LiuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
George BaylissDepartment of Medicine, Rhode Island Hospital, Alpert Medical School, Brown University, Providence, Rhode Island, U.S.A.
Shougang ZhuangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China szhuang@lifespan.org.ORCID 0000-0001-9719-4187
Brown University · USShanghai East Hospital · CN

Funding

Role of Histone Methyltransferase EZH2 in Acute and Chronic Renal InjuryR01DK113256 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2018 to 2021
$1.5M
NIDDK NIH HHS R01 DK113256
6 · The paper itself

Abstract

Nintedanib, a Food and Drug Administration-approved drug for the treatment of patients with idiopathic pulmonary fibrosis (IPK), inhibits both tyrosine kinase receptors and non-receptor kinases, and block activation of platelet-derived growth factor receptors, fibroblast growth factor receptor, vascular endothelial growth factor receptors, and Src family kinases. Preclinical and clinical studies have revealed the potent anti-fibrotic effect of nintedanib in IPK in human and animal models. Recent preclinical studies have also demonstrated the inhibitory effect of nintedanib on the development and progression of tissue fibrosis in other organs, including liver, kidney, and skin. The anti-fibrotic actions of nintedanib occur through a number of mechanisms, including blocking differentiation of fibroblasts to myofibroblasts, inhibition of epithelial-mesenchymal transition, and suppression of inflammation and angiogenesis. In this article, we summarize the mechanisms and efficacy of nintedanib in the treatment of fibrotic diseases in animal models and clinical trials, provide an update on recent advances in the development of other novel antifibrotic agents in preclinical and clinical study, and offer our perspective about the possible clinical application of these agents in fibrotic diseases.

Indexed as

AnimalsHumansIdiopathic Pulmonary FibrosisIndolesKidneyKidney DiseasesLiverLiver CirrhosisLungMolecular Targeted TherapyProtein Kinase InhibitorsSignal TransductionIndolesnintedanibProtein Kinase Inhibitorsangiogenesisepithelial-mesenchymal transitioninflammationmyofibroblastsNintedanibrenal fibrosis

Identifiers

PMID31217321
PMCPMC7480985
OpenAlexW2952521598

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.