Evidence map›Paper›PMID 31684100›Full record

ReviewJournal of clinical medicine2019

The Role of Protein SUMOylation in the Pathogenesis of Atherosclerosis.

Sajad Dehnavi, Mahvash Sadeghi, Peter E Penson, Maciej Banach, Tannaz Jamialahmadi, Amirhossein Sahebkar

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. SUMOylation targeting mitophagy in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  8. Signalling mechanisms and cellular functions of SUMO.Nature reviews. Molecular cell biology · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. HOPS and p53: thick as thieves in life and death.Cell cycle (Georgetown, Tex.) · 2020
    Review
  17. Review
  18. Review
  19. 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

6 authors at 4 institutions in 3 countries.

Sajad DehnaviDepartment of Immunology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 6135715794, Iran. dehnavis1@mailfa.com.
Mahvash SadeghiDepartment of Immunology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran. sadeghim1@mailfa.com.
Peter E PensonSchool of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK. P.Penson@ljmu.ac.uk.
Maciej BanachDepartment of Hypertension, WAM University Hospital in Lodz, Medical University of Lodz, Zeromskiego 113, Lodz 93-338, Poland. maciej.banach@icloud.com.
Tannaz JamialahmadiHalal Research Center of IRI, FDA, Tehran, Iran. jamialahmadit@mailfa.com.
Amirhossein SahebkarBiotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir.
Mashhad University of Medical Sciences · IRAhvaz Jundishapur University of Medical Sciences · IRLiverpool John Moores University · GBMedical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a progressive, inflammatory cardiovascular disorder characterized by the development of lipid-filled plaques within arteries. Endothelial cell dysfunction in the walls of blood vessels results in an increase in vascular permeability, alteration of the components of the extracellular matrix, and retention of LDL in the sub-endothelial space, thereby accelerating plaque formation. Epigenetic modification by SUMOylation can influence the surface interactions of target proteins and affect cellular functionality, thereby regulating multiple cellular processes. Small ubiquitin-like modifier (SUMO) can modulate NFκB and other proteins such as p53, KLF, and ERK5, which have critical roles in atherogenesis. Furthermore, SUMO regulates leukocyte recruitment and cytokine release and the expression of adherence molecules. In this review, we discuss the regulation by SUMO and SUMOylation modifications of proteins and pathways involved in atherosclerosis.

Indexed as

atherosclerosissmall ubiquitin-like modifier (SUMO)SUMOylation

Identifiers

PMID31684100
PMCPMC6912227
OpenAlexW2984956467

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.