Evidence map›Paper›PMID 28799781›Full record

ArticleAmerican journal of respiratory cell and molecular biology2017

MicroRNA-29c Prevents Pulmonary Fibrosis by Regulating Epithelial Cell Renewal and Apoptosis.

Ting Xie, Jiurong Liang, Yan Geng, Ningshan Liu, Adrianne Kurkciyan, Vrishika Kulur, Dong Leng, Nan Deng, Zhenqiu Liu, Jianbo Song and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  4. Article
  5. Article
  6. The complexities of cell death mechanisms: a new perspective in systemic sclerosis therapy.Apoptosis : an international journal on programmed cell death · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis.Journal of respiratory biology and translational medicine · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
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

13 authors at 2 institutions in 2 countries.

Ting Xie1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Jiurong Liang1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Yan Geng1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Ningshan Liu1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Adrianne Kurkciyan1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Vrishika Kulur1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Dong Leng2 Clinical Laboratory and Laboratory Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Nan Deng3 Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California; and.
Zhenqiu Liu3 Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California; and.
Jianbo Song4 Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Peter Chen1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Paul W Noble1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Dianhua Jiang1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Cedars-Sinai Medical Center · USCapital Medical University · CN

Funding

Role of Surfactant Proteins in Mediating Noninfectious Inflammatory and FibroproP01HL108793 · NHLBI · DUKE UNIVERSITY · PI STRIPP, BARRY R · 2012 to 2022
$21.3M
MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATIONR01HL060539 · NHLBI · YALE UNIVERSITY · PI NOBLE, PAUL WESLEY · 1997 to 2019
$6.5M
Innate Immune Mechanisms of Non-infectious Lung InflammationR01AI052201 · NIAID · YALE UNIVERSITY · PI NOBLE, PAUL WESLEY · 2002 to 2021
$6.4M
Targeting beta-arrestins in Pulmonary FibrosisR01HL122068 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI JIANG, DIANHUA, NOBLE, PAUL WESLEY · 2015 to 2018
$2.1M
NHLBI NIH HHS P01 HL108793NHLBI NIH HHS R01 HL060539NHLBI NIH HHS R01 HL122068NIAID NIH HHS R01 AI052201
6 · The paper itself

Abstract

Successful repair and renewal of alveolar epithelial cells (AECs) are critical in prohibiting the accumulation of myofibroblasts in pulmonary fibrogenesis. MicroRNAs (miRNAs) are multifocal regulators involved in lung injury and repair. However, the contribution of miRNAs to AEC2 renewal and apoptosis is incompletely understood. We report that miRNA-29c (miR-29c) expression is lower in AEC2s of individuals with idiopathic pulmonary fibrosis than in healthy lungs. Epithelial cells overexpressing miR-29c show higher proliferative rates and viability. miR-29c protects epithelial cells from apoptosis by targeting forkhead box O3a (Foxo3a). Both overexpression of miR-29c conventionally and AEC2s specifically lead to less fibrosis and better recovery in vivo. Furthermore, deficiency of miR-29c in AEC2s results in higher apoptosis and reduced epithelial renewal. Interestingly, a gene network including a subset of apoptotic genes was coregulated by both Toll-like receptor 4 and miR-29c. Taken together, miR-29c maintains epithelial integrity and promotes recovery from lung injury, thereby attenuating lung fibrosis in mice.

Indexed as

ApoptosisAnimalsEpithelial CellsFemaleHumansIdiopathic Pulmonary FibrosisMaleMiceMicroRNAsRespiratory MucosaToll-Like Receptor 4MicroRNAsMIRN29a microRNA, humanMIRN29 microRNA, mouseTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4alveolar epithelial type II cell apoptosisalveolar epithelial type II cell renewalmicroRNA-29cpulmonary fibrosis

Identifiers

PMID28799781
PMCPMC5765420
OpenAlexW2743863853

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.