Evidence map›Paper›PMID 29567124›Full record

ReviewMatrix biology : journal of the International Society for Matrix Biology2018

Endoplasmic reticulum stress in pulmonary fibrosis.

Ankita Burman, Harikrishna Tanjore, Timothy S Blackwell

Open access · greenAbstract readReview
In one paragraph

Review in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
16.7field-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

142 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. CYP1B1 modulates stress and repair pathways in airway cells challenged by wood smoke particles.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  8. IPF AT2 cells are stuck in transition and biophysically dysfunctional.bioRxiv : the preprint server for biology · 2026
    Article
  9. Review
  10. The intersection of liver cirrhosis and pulmonary fibrosis.Journal of translational medicine · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

82 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.

Ankita BurmanDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.
Harikrishna TanjoreDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
Timothy S BlackwellDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA; Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Veterans Affairs Medical Center, Nashville, TN, USA. Electronic address: timothy.blackwell@Vanderbilt.edu.
Vanderbilt University · US

Funding

Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BLACKWELL, TIMOTHY S. · 2010 to 2020
$21.6M
NHLBI NIH HHS P01 HL092870
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress is associated with development and progression of fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). ER stress was first implicated in the pathogenesis of IPF >15 years ago with the discovery of disease-causing mutations in surfactant protein C, which result in a misfolded gene product in type II alveolar epithelial cells (AECs). ER stress and the unfolded protein response (UPR) have been linked to lung fibrosis through regulation of AEC apoptosis, epithelial-mesenchymal transition, myofibroblast differentiation, and M2 macrophage polarization. Although progress has been made in understanding the causes and consequences of ER stress in IPF and a number of chronic fibrotic disorders, further studies are needed to identify key factors that induce ER stress in important cell types and define critical down-stream processes and effector molecules that mediate ER stress-related phenotypes. This review discusses potential causes of ER stress induction in the lungs and current evidence linking ER stress to fibrosis in the context of individual cell types: AECs, fibroblasts, and macrophages. As our understanding of the relationship between ER stress and lung fibrosis continues to evolve, future studies will examine new strategies to modulate UPR pathways for therapeutic benefit.

Indexed as

Endoplasmic Reticulum StressUnfolded Protein ResponseAlveolar Epithelial CellsAnimalsCell PolarityDisease ProgressionEpithelial-Mesenchymal TransitionHumansPulmonary Fibrosis

Identifiers

PMID29567124
PMCPMC6392005
OpenAlexW2790790936

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.