Evidence map›Paper›PMID 23092186›Full record

ReviewAnnual review of pathology2013

Host responses in tissue repair and fibrosis.

Jeremy S Duffield, Mark Lupher, Victor J Thannickal, Thomas A Wynn

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 334 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
334citing papers in PubMed, 2 pooled it
35.9field-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

334 citing papers in PubMed, 2 syntheses or guidelines pooled it, 620 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Review
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  10. Signal control during tissue regeneration in adult animals.Nature reviews. Molecular cell biology · 2026
    Review
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274 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

4 authors at 4 institutions in 1 country.

Jeremy S DuffieldDivision of Nephrology, Center for Lung Biology, and the Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98019, USA.
Mark Lupher
Victor J Thannickal
Thomas A Wynn
Melior Discovery (United States) · USNational Institutes of Health · USUniversity of Alabama at Birmingham · USUniversity of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Approaches To Immunological Intervention In SchistosomiasisZIAAI000829 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$9.9M
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
Oxidants and TGF-beta in Myofibroblast Differentiation/SurvivalR01HL067967 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THANNICKAL, VICTOR J. · 2001 to 2011
$2.7M
Pericyte-endothelial cross talk in vascular stability after kidney injuryR01DK093493 · NIDDK · UNIVERSITY OF WASHINGTON · PI SHANKLAND, STUART JAMES · 2012 to 2016
$2.5M
The role of Macrophage Delivered WNT Signaling in kidney injury and repairR01DK084077 · NIDDK · UNIVERSITY OF WASHINGTON · PI SHANKLAND, STUART JAMES · 2009 to 2013
$1.8M
Kidney pericytes in vascular regeneration after injuryRC1DK087389 · NIDDK · UNIVERSITY OF WASHINGTON · PI DUFFIELD, JEREMY S · 2009 to 2010
$989k
Rho-Kinase Pathway in Pulmonary FibrosisP50HL107181 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THANNICKAL, VICTOR J. · 2011 to 2012
$879k
Intramural NIH HHS ZIA AI000829Intramural NIH HHS ZIA AI001019NHLBI NIH HHS HL067967NHLBI NIH HHS HL107181NHLBI NIH HHS P50 HL107181NHLBI NIH HHS R01 HL067967NIDDK NIH HHS DK84077NIDDK NIH HHS DK87389NIDDK NIH HHS DK93493NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK084077NIDDK NIH HHS R01 DK093493NIDDK NIH HHS RC1 DK087389
6 · The paper itself

Abstract

Myofibroblasts accumulate in the spaces between organ structures and produce extracellular matrix (ECM) proteins, including collagen I. They are the primary "effector" cells in tissue remodeling and fibrosis. Previously, leukocyte progenitors termed fibrocytes and myofibroblasts generated from epithelial cells through epithelial-to-mesenchymal transition (EMT) were considered the primary sources of ECM-producing myofibroblasts in injured tissues. However, genetic fate mapping experiments suggest that mesenchyme-derived cells, known as resident fibroblasts, and pericytes are the primary precursors of scar-forming myofibroblasts, whereas epithelial cells, endothelial cells, and myeloid leukocytes contribute to fibrogenesis predominantly by producing key fibrogenic cytokines and by promoting cell-to-cell communication. Numerous cytokines derived from T cells, macrophages, and other myeloid cell populations are important drivers of myofibroblast differentiation. Monocyte-derived cell populations are key regulators of the fibrotic process: They act as a brake on the processes driving fibrogenesis, and they dismantle and degrade established fibrosis. We discuss the origins, modes of activation, and fate of myofibroblasts in various important fibrotic diseases and describe how manipulation of macrophage activation could help ameliorate fibrosis.

Indexed as

AnimalsCell CommunicationExtracellular MatrixFibrosisHumansMyofibroblastsPericytesWound Healing

Identifiers

PMID23092186
PMCPMC3789589
OpenAlexW2099486691

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.