Evidence map›Paper›PMID 27904144›Full record

ReviewNature reviews. Rheumatology2017

Causes and consequences of endoplasmic reticulum stress in rheumatic disease.

Fatemeh Navid, Robert A Colbert

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 106 citations in OpenAlex.

  1. Review
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  14. Review
  15. Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis.Clinical, cosmetic and investigational dermatology · 2024
    Review
  16. Insights into the structure and function of the RNA ligase RtcB.Cellular and molecular life sciences : CMLS · 2023
    Review
  17. Article
  18. Review
  19. Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023
    Review
  20. Article

2 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.

Fatemeh NavidPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health, Building 10, Room 12N248B,10 Center Drive, Bethesda, Maryland 20892, USA.
Robert A ColbertPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health, Building 10, Room 12N248B,10 Center Drive, Bethesda, Maryland 20892, USA.
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USNational Institutes of Health · US

Funding

Pathogenic Mechanisms in SpondyloarthritisZIAAR041184 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$47.6M
6 · The paper itself

Abstract

Rheumatic diseases represent a heterogeneous group of inflammatory conditions, many of which involve chronic activation of both innate and adaptive immune responses by multiple genetic and environmental factors. These immune responses involve the secretion of excessive amounts of cytokines and other signalling mediators by activated immune cells. The endoplasmic reticulum (ER) is the cellular organelle that directs the folding, processing and trafficking of membrane-bound and secreted proteins, including many key components of the immune response. Maintaining homeostasis in the ER is critical to cell function and survival. Consequently, elaborate mechanisms have evolved to sense and respond to ER stress through three main signalling pathways that together comprise the unfolded protein response (UPR). Activation of the UPR can rapidly resolve the accumulation of misfolded proteins, direct permanent changes in the size and function of cells during differentiation, and critically influence the immune response and inflammation. Recognition of the importance of ER stress and UPR signalling pathways in normal and dysregulated immune responses has greatly increased in the past few years. This Review discusses several settings in which ER stress contributes to the pathogenesis of rheumatic diseases and considers some of the therapeutic opportunities that these discoveries provide.

Indexed as

Activating Transcription Factor 6AnimalsAutoimmune DiseasesB-LymphocytesCell DifferentiationeIF-2 KinaseEndoplasmic Reticulum-Associated DegradationEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesHeat-Shock ProteinsHLA-B27 AntigenHumansMyocytes, Smooth MuscleProtein FoldingProtein Serine-Threonine KinasesActivating Transcription Factor 6eIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN1 protein, humanHeat-Shock ProteinsHLA-B27 AntigenProtein Serine-Threonine Kinases

Identifiers

PMID27904144
OpenAlexW2557340098

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.