Evidence map›Paper›PMID 22802289›Full record

ReviewProceedings of the American Thoracic Society2012

Genesis of the myofibroblast in lung injury and fibrosis.

Sem H Phan

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
9.0field-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

78 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
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  8. Article
  9. Article
  10. Mechanisms of prostatic inflammation-mediated male lower urinary tract symptoms.American journal of clinical and experimental urology · 2025
    Review
  11. Article
  12. The effect of adrenalectomy on bleomycin-induced pulmonary fibrosis in mice.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

18 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

1 author at 1 institution in 1 country.

Sem H PhanDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA. shphan@umich.edu
University of Michigan · US

Funding

MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1985 to 2009
$14.1M
MYOFIBROBLASTS IN PULMONARY FIBROSISR01HL052285 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1994 to 2017
$5.4M
Mechanisms of Pulmonary FibrosisR37HL028737 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 2001 to 2010
$3.0M
Novel telomerase expressing lung fibroblast phenotypeR01HL077297 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 2004 to 2012
$3.0M
MECHANISMS OF PULMONARY FIBROSISR01HL028737 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1986 to 2000
$227k
NHLBI NIH HHS HL28737NHLBI NIH HHS HL31963NHLBI NIH HHS HL52285NHLBI NIH HHS HL77297NHLBI NIH HHS HL91175NHLBI NIH HHS P01 HL031963NHLBI NIH HHS R01 HL028737NHLBI NIH HHS R01 HL052285NHLBI NIH HHS R01 HL077297NHLBI NIH HHS R37 HL028737
6 · The paper itself

Abstract

Tissue injury incites a repair response with a key mesenchymal component that provides the essential connective tissue for subsequent regeneration or pathological fibrosis. The fibroblast is the major mesenchymal cell type to be implicated in this connective tissue response, and it is in its activated or differentiated form that it participates in the repair process. The myofibroblast represents such an activated mesenchymal cell and is a key source of extracellular matrix and inflammatory/fibrogenic cytokines as well as participating in wound contraction. Although successful healing results in gradual disappearance of myofibroblasts, their persistence is associated with chronic and progressive fibrosis. Thus, elucidation of the mechanism involved in the genesis of the myofibroblast should provide insight into both pathogenesis of chronic fibrotic diseases and therapeutic strategies for their management and control. Although the fibroblast is a well-documented progenitor cell for the myofibroblast, recent studies have suggested additional precursor cells that have the potential to give rise to the myofibroblast. Many of the studies focused on mechanisms and factors that regulate induction of α-smooth muscle actin expression, a key and commonly used marker of the myofibroblast. These reveal complex and multifactorial mechanisms involving transcriptional and epigenetic regulation and implicating diverse cell-signaling pathways, including those activated by the potent fibrogenic cytokine transforming growth factor β. Despite these extensive studies, many aspects remain poorly understood, with the suggestion that additional novel mechanisms remain to be discovered. Future studies with the help of newly developed technical advancements should expedite discovery in this direction.

Indexed as

ActinsCell DifferentiationEpigenesis, GeneticEpithelial-Mesenchymal TransitionFibroblastsGene Expression RegulationHumansLung InjuryMesenchymal Stem CellsMyofibroblastsPulmonary FibrosisTransforming Growth Factor betaWound HealingActinsTransforming Growth Factor beta

Identifiers

PMID22802289
PMCPMC5830705
OpenAlexW1989970963

What OpenQuestion holds

Textmetadata
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.