Evidence map›Paper›PMID 23741300›Full record

ArticlePloS one2013

The triterpenoid CDDO-Me inhibits bleomycin-induced lung inflammation and fibrosis.

Ajit A Kulkarni, Thomas H Thatcher, Hsi-Min Hsiao, Keith C Olsen, Robert Matthew Kottmann, Jason Morrissette, Terry W Wright, Richard P Phipps, Patricia J Sime

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. [Bardoxolone methyl alleviates acute liver injury in mice by inhibiting NLRP3 inflammasome activation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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  8. Inhibiting Sialidase-Induced TGF-The Journal of pharmacology and experimental therapeutics · 2021
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  9. Review
  10. Article
  11. Review
  12. Review
  13. Attenuated pulmonary fibrosis in sialidase-3 knockout (American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

Ajit A KulkarniThe Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Rochester, Rochester, New York, United States of America.
Thomas H Thatcher
Hsi-Min Hsiao
Keith C Olsen
Robert Matthew Kottmann
Jason Morrissette
Terry W Wright
Richard P Phipps
Patricia J Sime
University of Rochester · US

Funding

Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
The University of Rochester's Clinical and Translational Science InstituteUL1TR000042 · NCATS · UNIVERSITY OF ROCHESTER · PI BENNETT, NANCY M, KIEBURTZ, KARL D. · 2012 to 2015
$14.4M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
The University of Rochester's Clinical and Translational Science InstituteKL2RR024136 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$4.3M
Modulation of Silica-Induced Pulmonary FibrosisR01HL075432 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2005 to 2009
$2.0M
Chemokine regulation of immune cell recruitment during Pneumocystis pneumoniaR01HL083761 · NHLBI · UNIVERSITY OF ROCHESTER · PI WRIGHT, TERRY W · 2006 to 2010
$2.0M
Macrophage effector functions during respiratory fungal infectionR01HL113495 · NHLBI · UNIVERSITY OF ROCHESTER · PI WRIGHT, TERRY W · 2012 to 2015
$1.5M
Role of T cells and PPARgamma in Graves' orbital fibroblast adipogenesisR01EY017123 · NEI · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P. · 2006 to 2010
$1.4M
Training in Biostatistics for HIV/AIDST32AI083206 · NIAID · UNIVERSITY OF ROCHESTER · PI QIU, XING · 2010 to 2014
$952k
NCATS NIH HHS 8UL1TR000042-07NCATS NIH HHS UL1 TR000042NCRR NIH HHS KL2 RR024136NCRR NIH HHS KL2RR024136NEI NIH HHS R01 EY017123NEI NIH HHS R01EY017123NHLBI NIH HHS R01 HL075432NHLBI NIH HHS R01HL075432NHLBI NIH HHS R01 HL083761NHLBI NIH HHS R01HL083761NHLBI NIH HHS R01 HL113495NHLBI NIH HHS T32 HL066988NHLBI NIH HHS T32HL066988NIAID NIH HHS T32 AI083206NIEHS NIH HHS T32 ES007026NIEHS NIH HHS T32ES007026
6 · The paper itself

Abstract

Pulmonary Fibrosis (PF) is a devastating progressive disease in which normal lung structure and function is compromised by scarring. Lung fibrosis can be caused by thoracic radiation, injury from chemotherapy and systemic diseases such as rheumatoid arthritis that involve inflammatory responses. CDDO-Me (Methyl 2-cyano-3,12-dioxooleana-1,9(11)dien-28-oate, Bardoxolone methyl) is a novel triterpenoid with anti-fibrotic and anti-inflammatory properties as shown by our in vitro studies. Based on this evidence, we hypothesized that CDDO-Me would reduce lung inflammation, fibrosis and lung function impairment in a bleomycin model of lung injury and fibrosis. To test this hypothesis, mice received bleomycin via oropharyngeal aspiration (OA) on day zero and CDDO-Me during the inflammatory phase from days -1 to 9 every other day. Bronchoalveolar lavage fluid (BALF) and lung tissue were harvested on day 7 to evaluate inflammation, while fibrosis and lung function were evaluated on day 21. On day 7, CDDO-Me reduced total BALF protein by 50%, alveolar macrophage infiltration by 40%, neutrophil infiltration by 90% (p≤0.01), inhibited production of the inflammatory cytokines KC and IL-6 by over 90% (p≤0.001), and excess production of the pro-fibrotic cytokine TGFβ by 50%. CDDO-Me also inhibited α-smooth muscle actin and fibronectin mRNA by 50% (p≤0.05). On day 21, CDDO-Me treatment reduced histological fibrosis, collagen deposition and αSMA production. Lung function was significantly improved at day 21 by treatment with CDDO-Me, as demonstrated by respiratory rate and dynamic compliance. These new findings reveal that CDDO-Me exhibits potent anti-fibrotic and anti-inflammatory properties in vivo. CDDO-Me is a potential new class of drugs to arrest inflammation and ameliorate fibrosis in patients who are predisposed to lung injury and fibrosis incited by cancer treatments (e.g. chemotherapy and radiation) and by systemic autoimmune diseases.

Indexed as

ActinsAdministration, InhalationAnimalsAnti-Inflammatory Agents, Non-SteroidalBleomycinBronchoalveolar Lavage FluidCollagenFibronectinsGene ExpressionHumansMacrophages, AlveolarMaleMiceMice, Inbred C57BLNeutrophil InfiltrationOleanolic AcidActinsalpha-smooth muscle actin, mouseAnti-Inflammatory Agents, Non-Steroidalbardoxolone methylBleomycinCollagenFibronectinsOleanolic AcidTransforming Growth Factor beta

Identifiers

PMID23741300
PMCPMC3669327
OpenAlexW2063025076

What OpenQuestion holds

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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.