Evidence map›Paper›PMID 22918530›Full record

ReviewCurrent opinion in rheumatology2012

The role of endoplasmic reticulum stress and the unfolded protein response in fibrosis.

Stefania Lenna, Maria Trojanowska

Abstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

73 citing papers in PubMed, 130 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  6. Article
  7. Article
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  9. Review
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  11. Effects of gas signaling molecule SOThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Article
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  18. Article
  19. Review
  20. Review

13 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 1 institution in 1 country.

Stefania LennaArthritis Center, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Maria Trojanowska
Boston University · US

Funding

Translational studies for identifying and targeting novel pathways in systemic sclerosis pathogenesisP50AR060780 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAFYATIS, ROBERT A. · 2011 to 2021
$14.9M
The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
TGF BETA RECEPTOR SIGNALING IN SCLERODERMAR01AR044883 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2012
$3.3M
NIAMS NIH HHS P50 AR060780NIAMS NIH HHS R01 AR042334NIAMS NIH HHS R01 AR044883NIAMS NIH HHS R01 AR42334NIAMS NIH HHS R01 AR44883
6 · The paper itself

Abstract

purpose of reviewTo review the present knowledge of the role of endoplasmic reticulum (ER) stress and unfolded protein response (UPR) in the pathogenesis of fibrotic diseases. RECENT

findingsER stress and UPR occur in a number of diseases associated with organ fibrosis; however, the contribution of these pathways to the fibrotic process has not been systematically investigated. Current studies suggest that prolonged ER stress may lead to fibrosis through activation of CCAAT/enhancer-binding homologous protein-mediated apoptosis, followed by an inflammatory response and release of profibrotic cytokines. A direct profibrotic role of UPR mediators in activation of TGF-β signaling has been shown in lung fibroblasts. In addition, activation of ER stress and UPR pathways in immune cells contributes to increased production of proinflammatory cytokines. SUMMARY: Although limited in scope, current studies strongly suggest that ER stress and UPR may play an important role during development of fibrosis. Further studies are warranted to gain additional insights into the relationship between these processes.

Indexed as

AnimalsApoptosisCCAAT-Enhancer-Binding ProteinsDisease Models, AnimalEndoplasmic Reticulum StressFibroblastsFibrosisHumansKidneyKidney DiseasesLungMyocytes, CardiacUnfolded Protein ResponseCCAAT-Enhancer-Binding Proteins

Identifiers

PMID22918530
PMCPMC3828639
OpenAlexW2059952390

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.