Evidence map›Paper›PMID 28439730›Full record

ReviewBasic research in cardiology2017

Physiological and therapeutic regulation of PCSK9 activity in cardiovascular disease.

Simon Glerup, Rainer Schulz, Ulrich Laufs, Klaus-Dieter Schlüter

Open access · hybridFull text readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Basic research in cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
10.7field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

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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

4 authors at 3 institutions in 2 countries.

Simon GlerupDepartment of Biomedicine, Aarhus University, 8000, Aarhus C, Denmark.
Rainer SchulzDepartment of Physiology, Justus-Liebig-University, Aulweg 129, 35392, Giessen, Germany.
Ulrich LaufsUniversitätsklinikum des Saarlandes, 66421, Homburg/Saar, Germany.
Klaus-Dieter SchlüterDepartment of Physiology, Justus-Liebig-University, Aulweg 129, 35392, Giessen, Germany. Klaus-Dieter.Schlueter@physiologie.med.uni-giessen.de.ORCID 0000-0002-6093-4919
Justus-Liebig-Universität Gießen · DEAarhus University · DKUniversitätsklinikum des Saarlandes · 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 is accelerated by increased levels of low-density lipoprotein cholesterol (LDL-C). Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a potent circulating regulator of LDL-C through its ability to induce degradation of the LDL receptor (LDLR) in the lysosome of hepatocytes. Only in the last few years, a number of breakthroughs in the understanding of PCSK9 biology have been reported illustrating how PCSK9 activity is tightly regulated at several levels by factors influencing its transcription, secretion, or by extracellular inactivation and clearance. Two humanized antibodies directed against the LDLR-binding site in PCSK9 received approval by the European and US authorities and additional PCSK9 directed therapeutics are climbing up the phases of clinical trials. The first outcome data of the PCSK9 inhibitor evolocumab reported a significant reduction in the composite endpoint (cardiovascular death, myocardial infarction, or stroke) and further outcome data are awaited. Meanwhile, it became evident that PCSK9 has (patho)physiological roles in several cardiovascular cells. In this review, we summarize and discuss the recent biological and clinical data on PCSK9, the regulation of PCSK9, its extra-hepatic activities focusing on cardiovascular cells, molecular concepts to target PCSK9, and finally briefly summarize the data of recent clinical studies.

Indexed as

AnimalsCardiovascular DiseasesHumansProprotein Convertase 9Receptors, LDLPCSK9 protein, humanProprotein Convertase 9Receptors, LDLLDLLDL receptoroxLDL

Identifiers

PMID28439730
PMCPMC5403857
OpenAlexW2610144433

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.