Evidence map›Paper›PMID 21861939›Full record

ReviewExpert reviews in molecular medicine2011

Myofibroblast differentiation and survival in fibrotic disease.

Kornelia Kis, Xiaoqiu Liu, James S Hagood

Open access · greenAbstract readReview
In one paragraph

Review in Expert reviews in molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 1 pooled it
10.2field-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

120 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
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  11. Review
  12. Article
  13. Article
  14. Review
  15. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

60 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

3 authors at 1 institution in 1 country.

Kornelia KisDepartment of Pediatrics, Division of Respiratory Medicine, University of California-San Diego, San Diego, CA, USA.
Xiaoqiu Liu
James S Hagood
University of California, San Diego · US

Funding

Regulation of Fibroblast Phenotype in Lung FibrosisR01HL082818 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAGOOD, JAMES S. · 2007 to 2017
$3.7M
Targeting the Apoptosis-Resistant Pulmonary MyofibroblastR01HL111169 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAGOOD, JAMES S. · 2012 to 2015
$1.7M
NHLBI NIH HHS HL 082818NHLBI NIH HHS R01 HL082818NHLBI NIH HHS R01 HL111169
6 · The paper itself

Abstract

During wound healing, contractile fibroblasts called myofibroblasts regulate the formation and contraction of granulation tissue; however, pathological and persistent myofibroblast activation, which occurs in hypertrophic scars or tissue fibrosis, results in a loss of function. Many reviews outline the cellular and molecular features of myofibroblasts and their roles in a variety of diseases. This review focuses on the origins of myofibroblasts and the factors that control their differentiation and prolonged survival in fibrotic tissues. Pulmonary fibrosis is used to illustrate many key points, but examples from other tissues and models are also included. Myofibroblasts originate mostly from tissue-resident fibroblasts, and also from epithelial and endothelial cells or other mesenchymal precursors. Their differentiation is influenced by cytokines, growth factors, extracellular matrix composition and stiffness, and cell surface molecules such as proteoglycans and THY1, among other factors. Many of these effects are modulated by cell contraction. Myofibroblasts resist programmed cell death, which promotes their accumulation in fibrotic tissues. The cause of resistance to apoptosis in myofibroblasts is under ongoing investigation, but many of the same stimuli that regulate their differentiation are involved. The contributions of oxidative stress, the WNT-β-catenin pathway and PPARγ to myofibroblast differentiation and survival are increasingly appreciated.

Indexed as

AnimalsCell DifferentiationHumansMyofibroblastsPulmonary Fibrosis

Identifiers

PMID21861939
PMCPMC5675569
OpenAlexW2016613783

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.