Evidence map›Paper›PMID 30367179›Full record

ReviewNature reviews. Endocrinology2018

Inhibiting PCSK9 - biology beyond LDL control.

Robert M Stoekenbroek, Gilles Lambert, Bertrand Cariou, G Kees Hovingh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
–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

72 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  8. HMGCR and Rosuvastatin Regulates GLP-1 Secretion and Expression-A Translational Study.The Journal of clinical endocrinology and metabolism · 2026
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  16. Observational
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12 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

4 authors.

Robert M StoekenbroekDepartment of Vascular Medicine, Academisch Medisch Centrum, Amsterdam, Netherlands.
Gilles LambertInserm UMR 1188 DéTROI, Université de La Réunion, Saint-Denis de La Réunion, France.
Bertrand CariouL'institut du thorax, INSERM, CNRS, Université de Nantes, CHU Nantes, Nantes, France.
G Kees HovinghDepartment of Vascular Medicine, Academisch Medisch Centrum, Amsterdam, Netherlands. g.k.hovingh@amc.uva.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical trials have unequivocally shown that inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) efficaciously and safely prevents cardiovascular events by lowering levels of LDL cholesterol. PCSK9 in the circulation is derived mainly from the liver, but the protein is also expressed in the pancreas, the kidney, the intestine and the central nervous system. Although PCSK9 modulates cholesterol metabolism by regulating LDL receptor expression in the liver, in vitro and in vivo studies have suggested that PCSK9 is involved in various other physiological processes. Although therapeutic PCSK9 inhibition could theoretically have undesired effects by interfering with these non-cholesterol-related processes, studies of individuals with genetically determined reduced PCSK9 function and clinical trials of PCSK9 inhibitors have not revealed clinically meaningful adverse consequences of almost completely eradicating PCSK9 from the circulation. The clinical implications of PCSK9 functions beyond lipid metabolism in terms of wanted or unwanted effects of therapeutic PCSK9 inhibition therefore appear to be limited. The objective of this Review is to describe the physiological role of PCSK9 beyond the LDL receptor to provide a rational basis for monitoring the effects of PCSK9 inhibition as these drugs gain traction in the clinic.

Indexed as

BiomarkersCardiovascular DiseasesCholesterol, LDLFemaleHumansHypercholesterolemiaLipid MetabolismMaleProprotein Convertase 9Receptors, LDLSensitivity and SpecificityBiomarkersCholesterol, LDLPCSK9 protein, humanProprotein Convertase 9Receptors, LDL

Identifiers

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.