Evidence map›Paper›PMID 25130181›Full record

ReviewIUBMB life2014

Endoplasmic reticulum stress and endothelial dysfunction.

Stefania Lenna, Rong Han, Maria Trojanowska

Open access · bronzeAbstract readReview
In one paragraph

Review in IUBMB life, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.5field-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

99 citing papers in PubMed, 161 citations in OpenAlex.

  1. Trial
  2. Article
  3. Atherosclerotic Cell Fates: A Single-Cell View of ER Stress.Journal of cardiovascular development and disease · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

39 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

3 authors at 1 institution in 1 country.

Stefania LennaArthritis Center, Boston University School of Medicine, Boston, MA, USA.
Rong Han
Maria Trojanowska
Boston University · US

Funding

WORK DISABILITY-- PERSONS WITH RHEUMATOID ARTHRITISP60AR047785 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FELSON, DAVID TOBIN · 2001 to 2016
$18.0M
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
RHEUMATOLOGY TRAINING GRANTT32AR007598 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FELSON, DAVID TOBIN · 1997 to 2018
$2.3M
NIAMS NIH HHS P50 AR060780NIAMS NIH HHS P60 AR047785NIAMS NIH HHS R01 AR042334NIAMS NIH HHS R01 AR04334NIAMS NIH HHS T32 AR007598
6 · The paper itself

Abstract

Prolonged perturbation of the endoplasmic reticulum (ER) leads to ER stress and unfolded protein response (UPR) and contributes to the pathogenesis of various chronic disorders. This review focuses on the role of ER stress and UPR in endothelial cells and the relevance of these processes to vascular diseases. Chronic activation of ER stress and UPR pathways in endothelial cells leads to increased oxidative stress and inflammation and often results in cell death. Because endothelial cells play a pivotal role in maintaining vascular homeostasis, various pathological conditions interfering with this homeostasis including homocysteinemia, hyperlipidemia, high glucose, insulin resistance, disturbed blood flow, and oxidative stress can lead to endothelial dysfunction in part through the activation of ER stress. We discuss recently discovered aspects of the role of ER stress/UPR in those pathological conditions. We also summarize recent findings implicating ER stress and UPR in systemic hypertension as well as pulmonary arterial hypertension. Finally, this review will highlight a novel role of UPR mediators in the process of angiogenesis.

Indexed as

Models, BiologicalEndoplasmic Reticulum StressEndothelial CellsHumansHyperhomocysteinemiaHyperlipidemiasHypertensionInflammationInsulin ResistanceNeovascularization, PathologicOxidative StressUnfolded Protein ResponseVascular Diseasescell deathcomplex diseasesJNKNF-kB/AP-1oxidative stressreactive oxygen species

Identifiers

PMID25130181
PMCPMC4181710
OpenAlexW2148441868

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.