Evidence map›Paper›PMID 34986654›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2022

miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.

Ashley R Rackow, Jennifer L Judge, Collynn F Woeller, Patricia J Sime, Robert M Kottmann

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025
    Article
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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

5 authors at 2 institutions in 1 country.

Ashley R RackowLung Biology and Disease Program, University of Rochester Medical Center Rochester, Rochester, New York.ORCID 0000-0002-4546-1455
Jennifer L JudgeCook MyoSite, Inc., Pittsburgh, Pennsylvania.
Collynn F WoellerDepartment of Environmental Medicine, University of Rochester Medical Center Rochester, Rochester, New York.
Patricia J SimeDivision of Pulmonary Disease and Critical Care Medicine, Virginia Commonwealth University, Richmond, Virginia.
Robert M KottmannLung Biology and Disease Program, University of Rochester Medical Center Rochester, Rochester, New York.ORCID 0000-0001-9316-6103
University of Rochester Medical Center · USVirginia Commonwealth University · US

Funding

MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
R01 Transfer from U. of Rochester- Lactate Promotes Scarring After IrradiationR01HL127001 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI SIME, PATRICIA JANET, WILLIAMS, JACQUELINE PATRICIA · 2016 to 2019
$1.5M
The lung epithelium is a source of lactate production in the pathogenesis of pulmonary fibrosisF31HL132453 · NHLBI · UNIVERSITY OF ROCHESTER · PI JUDGE, JENNIFER L. · 2016 to 2017
$51k
NHLBI NIH HHS F31 HL132453NHLBI NIH HHS R01 HL127001NHLBI NIH HHS T32 HL066988
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease. The pathogenesis of IPF is not completely understood. However, numerous genes are associated with the development and progression of pulmonary fibrosis, indicating there is a significant genetic component to the pathogenesis of IPF. Epigenetic influences on the development of human disease, including pulmonary fibrosis, remain to be fully elucidated. In this paper, we identify miR-338-3p as a microRNA severely downregulated in the lungs of patients with pulmonary fibrosis and in experimental models of pulmonary fibrosis. Treatment of primary human lung fibroblasts with miR-338-3p inhibits myofibroblast differentiation and matrix protein production. Published and proposed targets of miR-338-3p such as TGFβ receptor 1, MEK/ERK 1/2, Cdk4, and Cyclin D are also not responsible for the regulation of pulmonary fibroblast behavior by miR-338-3p. miR-338-3p inhibits myofibroblast differentiation by preventing TGFβ-mediated downregulation of phosphatase and tensin homolog (PTEN), a known antifibrotic mediator.

Indexed as

Idiopathic Pulmonary FibrosisMicroRNAsFibroblastsHumansLungMyofibroblastsPTEN PhosphohydrolaseTransforming Growth Factor betaMicroRNAsMIRN338 microRNA, humanPTEN PhosphohydrolasePTEN protein, humanTransforming Growth Factor betafibroblastlungmiRNApulmonary fibrosis

Identifiers

PMID34986654
PMCPMC8884407
OpenAlexW4205182106

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.