Evidence map›Paper›PMID 33053883›Full record

ReviewBiomedicines2020

Interplay between Endoplasmic Reticulum Stress and Large Extracellular Vesicles (Microparticles) in Endothelial Cell Dysfunction.

Aisha Osman, Tarek Benameur, Hesham M Korashy, Asad Zeidan, Abdelali Agouni

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Short-Term High-Intensity Treadmill Exercise Promotes Ceramide-Dependent Extracellular Vesicle Secretion in the Central Nervous System of Mice.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
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 2 institutions in 2 countries.

Aisha OsmanDepartment of Pharmaceutical Sciences, College of Pharmacy, QU health, Qatar University, Doha 2713, Qatar.ORCID 0000-0002-5015-6316
Tarek BenameurDepartment of Biomedical Sciences, College of Medicine, King Faisal University, P.O. Box 400, Al Ahsa 31982, Saudi Arabia.
Hesham M KorashyDepartment of Pharmaceutical Sciences, College of Pharmacy, QU health, Qatar University, Doha 2713, Qatar.ORCID 0000-0002-5745-9643
Asad ZeidanDepartment of Basic Medical Sciences, College of Medicine, QU health, Qatar University, Doha 2713, Qatar.
Abdelali AgouniDepartment of Pharmaceutical Sciences, College of Pharmacy, QU health, Qatar University, Doha 2713, Qatar.ORCID 0000-0002-8363-1582
Qatar University · QAKing Faisal University · SA

Funding

Qatar National Research Fund UREP24-016-3-004Qatar University QUCG-CPH-20/21-3Qatar University QUST-1-CPH-2018-1Qatar University QUST-2-CPH-2017-19
6 · The paper itself

Abstract

Upon increased demand for protein synthesis, accumulation of misfolded and/or unfolded proteins within the endoplasmic reticulum (ER), a pro-survival response is activated termed unfolded protein response (UPR), aiming at restoring the proper function of the ER. Prolonged activation of the UPR leads, however, to ER stress, a cellular state that contributes to the pathogenesis of various chronic diseases including obesity and diabetes. ER stress response by itself can result in endothelial dysfunction, a hallmark of cardiovascular disease, through various cellular mechanisms including apoptosis, insulin resistance, inflammation and oxidative stress. Extracellular vesicles (EVs), particularly large EVs (lEVs) commonly referred to as microparticles (MPs), are membrane vesicles. They are considered as a fingerprint of their originating cells, carrying a variety of molecular components of their parent cells. lEVs are emerging as major contributors to endothelial cell dysfunction in various metabolic disease conditions. However, the mechanisms underpinning the role of lEVs in endothelial dysfunction are not fully elucidated. Recently, ER stress emerged as a bridging molecular link between lEVs and endothelial cell dysfunction. Therefore, in the current review, we summarized the roles of lEVs and ER stress in endothelial dysfunction and discussed the molecular crosstalk and relationship between ER stress and lEVs in endothelial dysfunction.

Indexed as

cardiovascular diseasediabetesendoplasmic reticulum (ER) stressendothelial dysfunctionextracellular vesicles (EVs)metabolic syndromemicroparticles (MPs)

Identifiers

PMID33053883
PMCPMC7599704
OpenAlexW3092426938

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.