Evidence map›Paper›PMID 32635192›Full record

ArticleInternational journal of molecular sciences2020

The HSP90 Inhibitor, AUY-922, Ameliorates the Development of Nitrogen Mustard-Induced Pulmonary Fibrosis and Lung Dysfunction in Mice.

Pavel Solopov, Ruben M L Colunga Biancatelli, Margarita Marinova, Christiana Dimitropoulou, John D Catravas

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  5. The role of heat shock protein 90 in idiopathic pulmonary fibrosis: state of the art.European respiratory review : an official journal of the European Respiratory Society · 2025
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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

5 authors at 2 institutions in 2 countries.

Pavel SolopovFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.ORCID 0000-0002-1705-027X
Ruben M L Colunga BiancatelliFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
Margarita MarinovaFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
Christiana DimitropoulouFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
John D CatravasFrank Reidy Research Center for Bioelectrics, Old Dominion University, Norfolk, VA 23508, USA.
Old Dominion University · USPoliclinico Umberto I · IT

Funding

Antidotes against mustard-induced chronic lung injuryR21ES030528 · NIEHS · OLD DOMINION UNIVERSITY · PI CATRAVAS, JOHN D · 2018 to 2019
$426k
NIEHS NIH HHS R21 ES030528the CounterACT Program, National Institutes of Health Office of the Director (NIH OD) and the National Institute of Environmental Health Sciences (NIEHS) R21ES030528
6 · The paper itself

Abstract

Increased levels of heat shock protein 90 (HSP90) have been recently implicated in the pathogenesis of pulmonary fibrosis and the use of HSP90 inhibitors constitutes a potential therapeutic approach. Similarly, acute exposure to nitrogen mustard (NM) is related to the development of chronic lung injury driven by TNF-α, TGF-β, ERK and HSP90. Thus, we developed a murine model of NM-induced pulmonary fibrosis by instilling C57BI/6J mice with 0.625 mg/kg mechlorethamine hydrochloride. After 24 h, mice began receiving AUY-922, a second generation HSP90 inhibitor, at 1 mg/kg 2 times per week or 2 mg/kg 3 times per week, for either 10 or 30 days. AUY-922 suppressed the NM-induced sustained inflammation, as reflected in the reduction of leukocyte and protein concentrations in bronchoalveolar lavage fluid (BALF), and inhibited the activation of pro-fibrotic biomarkers, ERK and HSP90. Furthermore, AUY-922 maintained normal lung function, decreased the overexpression and accumulation of extracellular matrix proteins, and dramatically reduced histologic evidence of fibrosis in the lungs of mice exposed to NM. The HSP90 inhibitor, AUY-922, successfully blocked the adverse effects associated with acute exposures to NM, representing a promising approach against NM-induced pulmonary fibrosis.

Indexed as

AnimalsBiomarkersDisease Models, AnimalExtracellular Matrix ProteinsHSP90 Heat-Shock ProteinsIsoxazolesLungLung InjuryMaleMAP Kinase Signaling SystemMechlorethamineMiceMice, Inbred C57BLPulmonary AlveoliPulmonary FibrosisResorcinols5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamideBiomarkersExtracellular Matrix ProteinsHSP90 Heat-Shock ProteinsIsoxazolesMechlorethamineResorcinolsacute lung injuryanti-fibroticAUY-922ERKHSP90 inhibitorsnitrogen mustardP-HSP90pulmonary fibrosis

Identifiers

PMID32635192
PMCPMC7369861
OpenAlexW3038969721

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.