Evidence map›Paper›PMID 33062601›Full record

ReviewAdvanced pharmaceutical bulletin2020

PCSK9: A Key Target for the Treatment of Cardiovascular Disease (CVD).

Saeideh Sobati, Amir Shakouri, Mahdi Edalati, Daryoush Mohammadnejad, Reza Parvan, Javad Masoumi, Jalal Abdolalizadeh

Abstract readReview
In one paragraph

Review in Advanced pharmaceutical bulletin, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Effects of Cholesterol Modulation on Cisplatin-Induced Hearing Loss.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Antisense technology: an overview and prospectus.Nature reviews. Drug discovery · 2021
    Review
  17. 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

7 authors.

Saeideh SobatiDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Amir ShakouriDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mahdi EdalatiHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Daryoush MohammadnejadDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Reza ParvanDepartment of Biosciences, University of Milan, Via celoria 26, 20133, Milan, Italy.
Javad MasoumiImmunology Department, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Jalal AbdolalizadehImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID https://orcid.org/0000-0002-8283-5057

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9), as a vital modulator of low-density lipoprotein cholesterol (LDL-C) , is raised in hepatocytes and released into plasma where it binds to LDL receptors (LDLR), leading to their cleavage. PCSK9 adheres to the epidermal growth factor-like repeat A (EGF-A) domain of the LDLR which is confirmed by crystallography. LDLR expression is adjusted at the transcriptional level through sterol regulatory element binding protein 2 (SREBP-2) and at the post translational stages, specifically through PCSK9, and the inducible degrader of the LDLR PCSK9 inhibition is an appealing new method for reducing the concentration of LDL-C. In this review the role of PCSK9 in lipid homeostasis was elucidated, the effect of PCSK9 on atherosclerosis was highlighted, and contemporary therapeutic techniques that focused on PCSK9 were summarized. Several restoration methods to inhibit PCSK9 have been proposed which concentrate on both extracellular and intracellular PCSK9, and they include blockage of PCSK9 production by using gene silencing agents and blockage of it's binding to LDLR through antibodies and inhibition of PCSK9 autocatalytic processes by tiny molecule inhibitors.

Indexed as

AtherosclerosisCholesterolCoronary heart diseaseLDLMonoclonal antibodyPCSK9

Identifiers

PMID33062601
PMCPMC7539318

What OpenQuestion holds

Textmetadata
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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.