Evidence map›Paper›PMID 21668038›Full record

ReviewDrugs2011

New insights into the pathogenesis and treatment of idiopathic pulmonary fibrosis.

Qiang Ding, Tracy Luckhardt, Louise Hecker, Yong Zhou, Gang Liu, Veena B Antony, Joao deAndrade, Victor J Thannickal

Abstract readReview
In one paragraph

Review in Drugs, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed.

  1. S100A4 Orchestrates Fibroblast Fate to Drive Fibrotic Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  18. Focal adhesion kinase signaling determines the fate of lung epithelial cells in response to TGF-β.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
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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

8 authors.

Qiang DingDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, USA.
Tracy Luckhardt
Louise Hecker
Yong Zhou
Gang Liu
Veena B Antony
Joao deAndrade
Victor J Thannickal

Funding

The Role of FAK-related-non-kinase (FRNK) in Lung FibrosisR01HL085324 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DING, QIANG · 2007 to 2016
$3.9M
Oxidants and TGF-beta in Myofibroblast Differentiation/SurvivalR01HL067967 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THANNICKAL, VICTOR J. · 2001 to 2011
$2.7M
miR-21 and lung fibrosisR01HL105473 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIU, GANG · 2011 to 2015
$1.8M
Mass Spectrometry-Based Biomarker DiscoveryR01HL094230 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM, THANNICKAL, VICTOR J. · 2009 to 2012
$1.5M
HO-1 and granuloma formation in TB pleurisyR01AI080349 · NIAID · UNIVERSITY OF FLORIDA · PI ANTONY, VEENA B. · 2009 to 2010
$731k
TLR9 Activation and Fibrotic Responses in Alveolar Epithelial CellsK08HL094666 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUCKHARDT, TRACY R · 2009 to 2013
$669k
MicroRNAs, inflammation, and acute lung injury.R21HL097218 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIU, GANG · 2010 to 2011
$403k
Regulation of Mechano-Induced TGFb1 Activation and Myofibroblast DifferentiationR21HL097215 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHOU, YONG · 2009 to 2010
$403k
NHLBI NIH HHS K08 HL094666NHLBI NIH HHS R01 HL067967NHLBI NIH HHS R01HL067967NHLBI NIH HHS R01 HL085324NHLBI NIH HHS R01 HL094230NHLBI NIH HHS R01 HL105473NHLBI NIH HHS R21 HL097215NHLBI NIH HHS R21 HL097218NIAID NIH HHS R01 AI080349
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is the most common and lethal of the idiopathic interstitial pneumonias. There are currently no effective pharmacological therapies approved for the treatment of IPF. Despite the focus on targeting fibrogenic pathways, recent clinical trials have been largely disappointing. Progress is being made in elucidating key cellular processes and molecular pathways critical to IPF pathogenesis, and this should facilitate the development of more effective therapeutics for this recalcitrant disease. Emerging pathobiological concepts include the role of aging and cellular senescence, oxidative stress, endoplasmic reticulum stress, cellular plasticity, microRNAs and mechanotransduction. Therapeutic approaches that target molecular pathways to modulate aberrant cellular phenotypes and promote tissue homeostasis in the lung must be developed. Heterogeneity in biological and clinical phenotypes of IPF warrants a personalized medicine approach to diagnosis and treatment of this lung disorder.

Indexed as

AnimalsHumansIdiopathic Pulmonary FibrosisMolecular Targeted TherapyRisk Factors

Identifiers

PMID21668038
PMCPMC3955181

What OpenQuestion holds

Textmetadata
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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.