Evidence map›Paper›PMID 29293089›Full record

ReviewThe Journal of clinical investigation2018

Endoplasmic reticulum stress in the pathogenesis of fibrotic disease.

Jonathan A Kropski, Timothy S Blackwell

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 1 pooled it
11.3field-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

127 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. IPF AT2 cells are stuck in transition and biophysically dysfunctional.bioRxiv : the preprint server for biology · 2026
    Article
  11. Diabetes and cancer: therapeutic implications.Cardio-oncology (London, England) · 2026
    Review
  12. Review
  13. Article
  14. Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

67 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

2 authors at 2 institutions in 1 country.

Jonathan A KropskiDivision of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Timothy S BlackwellDivision of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BLACKWELL, TIMOTHY S. · 2010 to 2020
$21.6M
Interdisciplinary Training Program in Lung ResearchT32HL094296 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ray Stokes Peebles · 2008 to 2026
$6.3M
RLDC: Molecular Pathway-Driven Diagnostics & Therapeutics for Rare Lung DiseasesU54HL127672 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI TRAPNELL, BRUCE C · 2014 to 2018
$3.7M
Epithelial-Fibroblast Interactions in Lung FibrosisR01HL085317 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S. · 2007 to 2015
$3.5M
DNA-Damage Repair In Pulmonary FibrosisK08HL130595 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KROPSKI, JONATHAN ANDREW · 2016 to 2020
$786k
NHLBI NIH HHS K08 HL130595NHLBI NIH HHS P01 HL092870NHLBI NIH HHS R01 HL085317NHLBI NIH HHS T32 HL094296NHLBI NIH HHS U54 HL127672
6 · The paper itself

Abstract

Eukaryotic cells contain an elegant protein quality control system that is crucial in maintaining cellular homeostasis; however, dysfunction of this system results in endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR). Severe or prolonged ER stress is associated with the development of degenerative and fibrotic disorders in multiple organs, as evidenced by the identification of disease-causing mutations in epithelial-restricted genes that lead to protein misfolding or mistrafficking in familial fibrotic diseases. Emerging evidence implicates ER stress and UPR signaling in a variety of profibrotic mechanisms in individual cell types. In epithelial cells, ER stress can induce apoptosis, inflammatory signaling, and epithelial-mesenchymal transition. In other cell types, ER stress is linked to myofibroblast activation, macrophage polarization, and T cell differentiation. ER stress-targeted therapies have begun to emerge using approaches that range from global enhancement of chaperone function to selective targeting of activated ER stress sensors and other downstream mediators. As the complex regulatory mechanisms of this system are further clarified, there are opportunities to develop new disease-modifying therapeutic strategies in a wide range of chronic fibrotic diseases.

Indexed as

ApoptosisEndoplasmic Reticulum StressSignal TransductionUnfolded Protein ResponseAnimalsFibrosisHumansInflammationMacrophagesMolecular ChaperonesMyofibroblastsMolecular Chaperones

Identifiers

PMID29293089
PMCPMC5749533
OpenAlexW2782133916

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.