Evidence map›Paper›PMID 28335520›Full record

ReviewInternational journal of molecular sciences2017

Endoplasmic Reticulum Stress and Unfolded Protein Response in Cartilage Pathophysiology; Contributing Factors to Apoptosis and Osteoarthritis.

Alexandria Hughes, Alexandra E Oxford, Ken Tawara, Cheryl L Jorcyk, Julia Thom Oxford

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Osmolarity-Induced Altered Intracellular Molecular Crowding Drives Osteoarthritis Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  17. Article
  18. Review
  19. Review
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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

5 authors at 1 institution in 1 country.

Alexandria HughesDepartment of Biological Sciences, Boise State University, Boise, ID 83725, USA. alexhughes1@u.boisestate.edu.
Alexandra E OxfordDepartment of Biological Sciences, Boise State University, Boise, ID 83725, USA. aliceoxford@u.boisestate.edu.
Ken TawaraBiomolecular Sciences Graduate Program, Boise State University, Boise, ID 83725, USA. kentawara@u.boisestate.edu.
Cheryl L JorcykDepartment of Biological Sciences, Boise State University, Boise, ID 83725, USA. cjorcyk@boisestate.edu.
Julia Thom OxfordDepartment of Biological Sciences, Boise State University, Boise, ID 83725, USA. joxford@boisestate.edu.
Boise State University · US

Funding

Women's health: interplay of maternal diet and key demographics on neurological health in the rural frontier and remote WestP20GM103408 · NIGMS · UNIVERSITY OF IDAHO · PI Scott A Minnich · 2012 to 2026
$59.8M
VPS35 D620N inhibits autophagy through disrupted hyaluronic acid-CD44 signalingP20GM109095 · NIGMS · BOISE STATE UNIVERSITY · PI OXFORD, JULIA THOM · 2014 to 2023
$22.7M
NIGMS NIH HHS P20 GM103408NIGMS NIH HHS P20 GM109095
6 · The paper itself

Abstract

Chondrocytes of the growth plate undergo apoptosis during the process of endochondral ossification, as well as during the progression of osteoarthritis. Although the regulation of this process is not completely understood, alterations in the precisely orchestrated programmed cell death during development can have catastrophic results, as exemplified by several chondrodystrophies which are frequently accompanied by early onset osteoarthritis. Understanding the mechanisms that underlie chondrocyte apoptosis during endochondral ossification in the growth plate has the potential to impact the development of therapeutic applications for chondrodystrophies and associated early onset osteoarthritis. In recent years, several chondrodysplasias and collagenopathies have been recognized as protein-folding diseases that lead to endoplasmic reticulum stress, endoplasmic reticulum associated degradation, and the unfolded protein response. Under conditions of prolonged endoplasmic reticulum stress in which the protein folding load outweighs the folding capacity of the endoplasmic reticulum, cellular dysfunction and death often occur. However, unfolded protein response (UPR) signaling is also required for the normal maturation of chondrocytes and osteoblasts. Understanding how UPR signaling may contribute to cartilage pathophysiology is an essential step toward therapeutic modulation of skeletal disorders that lead to osteoarthritis.

Indexed as

ApoptosisEndoplasmic Reticulum StressUnfolded Protein ResponseAge of OnsetAnimalsArthritisBone Morphogenetic ProteinsCalcification, PhysiologicCartilageChondrocytesChondrogenesisCollagenConnective Tissue DiseasesEndoplasmic ReticulumHearing Loss, SensorineuralHumansBone Morphogenetic ProteinsCollagenchondrocyteendochondral ossificationendoplasmic reticulum (ER) stressosteoarthritisunfolded protein response

Identifiers

PMID28335520
PMCPMC5372677
OpenAlexW2600568230

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.