Evidence map›Paper›PMID 19851784›Full record

ReviewCell and tissue research2010

The unfolded protein response and its relevance to connective tissue diseases.

Raymond P Boot-Handford, Michael D Briggs

Open access · hybridAbstract readReview
In one paragraph

Review in Cell and tissue research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

82 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Glutamine-dependent changes in fibroblast-derived extracellular matrix dictate cancer cell behavior.Matrix biology : journal of the International Society for Matrix Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. The role of periostin in cardiac fibrosis.Heart failure reviews · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Ribosome dysfunction in osteoarthritis.Current opinion in rheumatology · 2022
    Review
  19. Review
  20. Expression of Human Mutant Preproinsulins Induced Unfolded Protein Response,International journal of molecular sciences · 2021
    Article

22 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.

Raymond P Boot-HandfordWellcome Trust Centre for Cell-Matrix Research, The University of Manchester, UK. ray.boot-handford@manchester.ac.uk
Michael D Briggs
University of Manchester · GBWellcome Centre for Cell-Matrix Research · GB

Funding

Targeted mouse models for studying skeletal dysplasiaR01AR049547 · NIAMS · UNIVERSITY OF MANCHESTER · PI BRIGGS, MICHAEL D · 2002 to 2005
$728k
NIAMS NIH HHS R01 AR049547NIAMS NIH HHS R01 AR49547-01Wellcome Trust 084353Wellcome Trust 084353/Z/07/Z
6 · The paper itself

Abstract

The unfolded protein response (UPR) has evolved to counter the stresses that occur in the endoplasmic reticulum (ER) as a result of misfolded proteins. This sophisticated quality control system attempts to restore homeostasis through the action of a number of different pathways that are coordinated in the first instance by the ER stress-senor proteins IRE1, ATF6 and PERK. However, prolonged ER-stress-related UPR can have detrimental effects on cell function and, in the longer term, may induce apoptosis. Connective tissue cells such as fibroblasts, osteoblasts and chondrocytes synthesise and secrete large quantities of proteins and mutations in many of these gene products give rise to heritable disorders of connective tissues. Until recently, these mutant gene products were thought to exert their effect through the assembly of a defective extracellular matrix that ultimately disrupted tissue structure and function. However, it is now becoming clear that ER stress and UPR, because of the expression of a mutant gene product, is not only a feature of, but may be a key mediator in the initiation and progression of a whole range of different connective tissue diseases. This review focuses on ER stress and the UPR that characterises an increasing number of connective tissue diseases and highlights novel therapeutic opportunities that may arise.

Indexed as

Unfolded Protein ResponseActivating Transcription Factor 6AnimalsApoptosisChondrocytesConnective Tissue DiseaseseIF-2 KinaseEndoplasmic ReticulumEndoribonucleasesFibroblastsGene Expression RegulationHomeostasisHumansMembrane ProteinsOsteoblastsProtein Serine-Threonine KinasesActivating Transcription Factor 6ATF6 protein, humaneIF-2 KinaseEndoribonucleasesERN2 protein, humanMembrane ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID19851784
PMCPMC2784867
OpenAlexW2016131399

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.