Evidence map›Paper›PMID 36768292›Full record

ReviewInternational journal of molecular sciences2023

PCSK9 as an Atherothrombotic Risk Factor.

Tadeja Sotler, Miran Šebeštjen

Open access · goldFull text readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
6.0field-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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. PCSK9 Inhibitors: The Evolving Future.Health science reports · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
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.

Tadeja SotlerDepartment of Cardiology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.
Miran ŠebeštjenDepartment of Cardiology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.ORCID 0000-0001-9907-3522
Ljubljana University Medical Centre · SIUniversity of Ljubljana · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disturbances in lipid metabolism are among the most important risk factors for atherosclerotic cardiovascular disease. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key protein in lipid metabolism that is also involved in the production of inflammatory cytokines, endothelial dysfunction and aherosclerotic plaque development. Studies have shown a connection between PCSK9 and various indicators of inflammation. Signalling pathways that include PCSK9 play important role in the initiation and development of atherosclerotic lesions by inducing vascular inflammation. Studies so far have suggested that PCSK9 is associated with procoagulation, enhancing the development of atherosclerosis. Experimentally, it was also found that an increased concentration of PCSK9 significantly accelerated the apoptosis of endothelial cells and reduced endothelial function, which created conditions for the development of atherosclerosis. PCSK9 inhibitors can therefore improve clinical outcomes not only in a lipid-dependent manner, but also through lipid-independent pathways. The aim of our review was to shed light on the impact of PCSK9 on these factors, which are not directly related to low-density lipoprotein (LDL) cholesterol metabolism.

Indexed as

AtherosclerosisProprotein Convertase 9Endothelial CellsHumansInflammationLipoproteins, LDLRisk FactorsLipoproteins, LDLPCSK9 protein, humanProprotein Convertase 9atherosclerosiscoagulationinflammationLDL cholesterolPCSK9

Identifiers

PMID36768292
PMCPMC9916735
OpenAlexW4317425565

What OpenQuestion holds

Textfull text, public
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.