Evidence map›Paper›PMID 25544176›Full record

ReviewAtherosclerosis2015

On the function and homeostasis of PCSK9: reciprocal interaction with LDLR and additional lipid effects.

Hagai Tavori, Shirya Rashid, Sergio Fazio

Open access · greenAbstract readReview
In one paragraph

Review in Atherosclerosis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Review
  3. Engineered extracellular vesicles as nanosponges for lysosomal degradation of PCSK9.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  4. PCSK9 Inhibitors: The Evolving Future.Health science reports · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. The role of lipid metabolism in cancer radioresistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Low circulating PCSK9 levels inFrontiers in genetics · 2022
    Article
  17. Old and New Calcineurin Inhibitors in Lupus Nephritis.Journal of clinical medicine · 2021
    Review
  18. Article
  19. Molecules (Basel, Switzerland) · 2021
    Article
  20. 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

3 authors at 2 institutions in 2 countries.

Hagai TavoriThe Knight Cardiovascular Institute, Center of Preventive Cardiology, Oregon Health and Sciences University, Portland, OR, USA.
Shirya RashidDepartment of Pharmacology, Dalhousie University, Halifax, Nova Scotia, and Saint John, New Brunswick, Canada.
Sergio FazioThe Knight Cardiovascular Institute, Center of Preventive Cardiology, Oregon Health and Sciences University, Portland, OR, USA. Electronic address: fazio@ohsu.edu.
Dalhousie University · CAOregon Health & Science University · US

Funding

PCSK9, Lipoprotein receptors, and AtherosclerosisR01HL106845 · NHLBI · VANDERBILT UNIVERSITY · PI FAZIO, SERGIO · 2011 to 2014
$2.0M
NHLBI NIH HHS R01 HL106845NHLBI NIH HHS R01-HL106845
6 · The paper itself

Abstract

Proprotein convertase subtilisin kexin type 9 (PCSK9) is a circulatory ligand that terminates the lifecycle of the low-density lipoprotein (LDL) receptor (LDLR) thus affecting plasma LDL-cholesterol (LDL-C) levels. Recent evidence shows that in addition to the straightforward mechanism of action, there are more complex interactions between PCSK9, LDLR and plasma lipoprotein levels, including: (a) the presence of both parallel and reciprocal regulation of surface LDLR and plasma PCSK9; (b) a correlation between PCSK9 and LDL-C levels dependent not only on the fact that PCSK9 removes hepatic LDLR, but also due to the fact that up to 40% of plasma PCSK9 is physically associated with LDL; and (c) an association between plasma PCSK9 production and the assembly and secretion of triglyceride-rich lipoproteins. The effect of PCSK9 on LDLR is being successfully utilized toward the development of anti-PCSK9 therapies to reduce plasma LDL-C levels. Current biochemical research has uncovered additional mechanisms of action and interacting partners for PCSK9, and this opens the way for a more thorough understanding of the regulation, metabolism, and effects of this interesting protein.

Indexed as

Lipid MetabolismAnimalsCholesterol, LDLDyslipidemiasEnzyme InhibitorsHomeostasisHumansHypolipidemic AgentsMolecular Targeted TherapyProprotein Convertase 9Proprotein ConvertasesProtein BindingReceptors, LDLSerine EndopeptidasesTriglyceridesCholesterol, LDLEnzyme InhibitorsHypolipidemic AgentsPCSK9 protein, humanProprotein Convertase 9Proprotein ConvertasesReceptors, LDLSerine EndopeptidasesTriglyceridesLow-density lipoproteinLow-density lipoprotein receptorPleiotropic effectsProprotein convertase subtilisin kexin 9Protein interaction

Identifiers

PMID25544176
PMCPMC4562333
OpenAlexW2086048382

What OpenQuestion holds

Texttitle and abstract
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.