Evidence map›Paper›PMID 28176216›Full record

ReviewClinical research in cardiology supplements2017

PCSK9 targets important for lipid metabolism.

Rainer Schulz, Klaus-Dieter Schlüter

Open access · hybridFull text readReview
In one paragraph

Review in Clinical research in cardiology supplements, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.2field-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

23 citing papers in PubMed, 60 citations in OpenAlex.

  1. PCSK9 and Breast Cancer Survival: A Mendelian Randomization Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
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  15. An Update on the Role of PCSK9 in Atherosclerosis.Journal of atherosclerosis and thrombosis · 2020
    Review
  16. Review
  17. Review
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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 1 institution in 1 country.

Rainer SchulzDepartment of Physiology, Justus-Liebig-Universität, Aulweg 129, 35392, Giessen, Germany. rainer.schulz@physiologie.med.uni-giessen.de.
Klaus-Dieter SchlüterDepartment of Physiology, Justus-Liebig-Universität, Aulweg 129, 35392, Giessen, Germany.
University of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic heart disease is the main cause of death worldwide and it is accelerated by increased low-density lipoprotein (LDL) cholesterol (LDL-C) and/or lipoprotein (a) (Lp(a)) concentrations. Proprotein convertase subtilisin/kexin type 9 (PCSK9) alters both LDL-C and in part Lp(a) concentrations through its ability to induce degradation of the LDL receptor (LDLR). PCSK9, however, has additional targets which are potentially involved in lipid metabolism regulation such as the very low density lipoprotein receptor (VLDL), CD36 (cluster of differentiation 36) and the epithelial cholesterol transporter (NPC1L1) and it affects expression of apolipoprotein B48. The PCSK9 activity is tightly regulated at several levels by factors influencing its transcription, secretion, or by extracellular inactivation and clearance. Many comorbidities (kidney insufficiency, hypothyreoidism, hyperinsulinemia, inflammation) modify PCSK9 expression and release. Two humanized antibodies directed against extracellular PCSK9 received approval by the European and US authorities and additional PCSK9 directed therapeutics (such as silencing RNA) are already in clinical trials. Their results demonstrate a significant reduction in both LDL-C and Lp(a) concentrations - independent of the concomitant medication - and one of them reduced plaque size in high risk cardiovascular patients; results of two ongoing large clinical endpoints studies are awaited. In this review, we summarize and discuss the recent biological data on PCSK9, the regulation of PCSK9, and finally briefly summarize the data of recent clinical studies in the context of lipid metabolism.

Indexed as

PCSK9 InhibitorsRNAi TherapeuticsAnimalsBiomarkersCardiovascular DiseasesCholesterol, LDLDyslipidemiasHumansHypolipidemic AgentsLipid MetabolismLipoprotein(a)Molecular Targeted TherapyProprotein Convertase 9Risk FactorsSerine Proteinase InhibitorsTreatment OutcomeBiomarkersCholesterol, LDLHypolipidemic AgentsLipoprotein(a)PCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Serine Proteinase InhibitorsLDL receptorLipoprotein (a)Low density lipoprotein (LDL)

Identifiers

PMID28176216
PMCPMC5352789
OpenAlexW2586272713

What Socratic holds

Textfull text, public
LicenceCC BY
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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 Socratic graph.