Evidence map›Paper›PMID 23602652›Full record

ReviewCurrent opinion in pharmacology2013

Pathogenesis, current treatments and future directions for idiopathic pulmonary fibrosis.

Hillary Loomis-King, Kevin R Flaherty, Bethany B Moore

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
10.0field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 97 citations in OpenAlex.

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  18. NMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  19. Fatty acid synthase is required for profibrotic TGF-β signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    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

3 authors at 1 institution in 1 country.

Hillary Loomis-KingDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Kevin R Flaherty
Bethany B Moore
University of Michigan–Ann Arbor · US

Funding

Periostin Regulation of Lung FibrosisR01HL115618 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2013 to 2016
$1.6M
Herpesvirus infection/injury govern fibrocyte recruitment and activationR01HL087846 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2008 to 2011
$1.5M
Fibrocyte Phenotypes as Biomarkers in IPFnet PatientsR01HL091745 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2008 to 2011
$1.4M
Forging a road to personalized medicine in interstitial lung diseasesK24HL111316 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FLAHERTY, KEVIN R · 2012 to 2017
$909k
NHLBI NIH HHS HL091745NHLBI NIH HHS K24 HL111316NHLBI NIH HHS R01 HL087846NHLBI NIH HHS R01 HL091745NHLBI NIH HHS R01 HL115618
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease (ILD) of unknown origin characterized by epithelial cell dysfunctions, accumulation of fibroblasts and myofibroblasts and relentless deposition of extracellular matrix (ECM). Improved diagnostic accuracy and better trial design have provided important insights from recent clinical trials. Perhaps the most important insight was the realization that 'standard therapy' was actually harmful! This review summarizes the current understanding of the cell types that are altered in IPF and the pathogenic mechanisms that have been identified. It also reviews recent clinical trial results and interpretations. Finally, we highlight attractive biologic targets and therapies in development with recommendations for future therapeutic avenues.

Indexed as

Idiopathic Pulmonary FibrosisAnimalsComorbidityFamilial Primary Pulmonary HypertensionGastroesophageal RefluxHumansHypertension, Pulmonary

Identifiers

PMID23602652
PMCPMC3686907
OpenAlexW1970120381

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.