Evidence map›Paper›PMID 22772564›Full record

ReviewNature medicine2012

Mechanisms of fibrosis: therapeutic translation for fibrotic disease.

Thomas A Wynn, Thirumalai R Ramalingam

Abstract readReview
In one paragraph

Review in Nature medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,987 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,987citing papers in PubMed, 2 pooled it
110.9field-weighted citation impact, top 1% 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

1,987 citing papers in PubMed, 2 syntheses or guidelines pooled it, 3,390 citations in OpenAlex.

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  10. Reversal of injury-induced fibrosis and anal sphincter muscle dysfunction by sFRP2 in rabbits.American journal of physiology. Gastrointestinal and liver physiology · 2026
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1,927 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Thomas A WynnImmunopathogenesis Section, Program in Barrier Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. twynn@niaid.nih.gov
Thirumalai R Ramalingam
National Institutes of Health · US

Funding

Mechanisms of Fibrosis in Asthma and Other Fibroproliferative DiseasesZIAAI001019 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$7.1M
Intramural NIH HHS ZIA AI001019
6 · The paper itself

Abstract

Fibrosis is a pathological feature of most chronic inflammatory diseases. Fibrosis, or scarring, is defined by the accumulation of excess extracellular matrix components. If highly progressive, the fibrotic process eventually leads to organ malfunction and death. Fibrosis affects nearly every tissue in the body. Here we discuss how key components of the innate and adaptive immune response contribute to the pathogenesis of fibrosis. We also describe how cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix-producing myofibroblasts. Finally, we highlight some of the key mechanisms and pathways of fibrosis that are being targeted as potential therapies for a variety of important human diseases.

Indexed as

Translational Research, BiomedicalFibrosisHumansImmunityInflammation MediatorsMyofibroblastsWound HealingInflammation Mediators

Identifiers

PMID22772564
PMCPMC3405917
OpenAlexW2045142779

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.