Evidence map›Paper›PMID 22811413›Full record

ReviewJournal of lipid research2012

The PCSK9 decade.

Gilles Lambert, Barbara Sjouke, Benjamin Choque, John J P Kastelein, G Kees Hovingh

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 8 pooled it
37.0field-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

192 citing papers in PubMed, 8 syntheses or guidelines pooled it, 442 citations in OpenAlex.

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  4. Biotechnology Approaches for the Treatment of Dyslipidemia.Cardiovascular drugs and therapy · 2021
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132 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 3 countries.

Gilles LambertLaboratoire Inserm U957, Université de Nantes, Faculté de Médecine, Nantes, France.
Barbara Sjouke
Benjamin Choque
John J P Kastelein
G Kees Hovingh
Academic Medical Center · NLInserm · FRThe Heart Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PCSK9 proprotein convertase subtilisin/kexin type (PCSK9) is a crucial protein in LDL cholesterol (LDL-C) metabolism by virtue of its pivotal role in the degradation of the LDL receptor. In recent years, both in vitro and in vivo studies have greatly supplemented our understanding of the (patho)physiological role of PCSK9 in human biology. In the current review, we summarize studies published or in print before May 2012 concerning the physiological role of PCSK9 in cholesterol metabolism. Moreover, we briefly describe the clinical phenotypes encountered in carriers of mutations in the gene encoding PCSK9. As PCSK9 has emerged as a novel target for LDL-C lowering therapy, methods to inhibit PCSK9 will also be reviewed. Initial data from investigations of PCSK9 inhibition in humans are promising and indicate that PCSK9 inhibition may be a viable new therapeutic option for the treatment of dyslipidemia and associated cardiovascular diseases.

Indexed as

Proprotein ConvertasesSerine EndopeptidasesAnticholesteremic AgentsCardiovascular DiseasesCholesterolDyslipidemiasHumansHydroxymethylglutaryl-CoA Reductase InhibitorsPhenotypeProprotein Convertase 9Anticholesteremic AgentsCholesterolHydroxymethylglutaryl-CoA Reductase InhibitorsPCSK9 protein, humanProprotein Convertase 9Proprotein ConvertasesSerine Endopeptidases

Identifiers

PMID22811413
PMCPMC3494258
OpenAlexW2043461445

What OpenQuestion holds

Texttitle and abstract
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.