Evidence map›Paper›PMID 34659352›Full record

ArticleFrontiers in genetics2021

Genome-Wide Association of Proprotein Convertase Subtilisin/Kexin Type 9 Plasma Levels in the ELSA-Brasil Study.

Isabela Bensenor, Kallyandra Padilha, Isabella Ramos Lima, Raul Dias Santos, Gilles Lambert, Stéphane Ramin-Mangata, Marcio S Bittencourt, Alessandra C Goulart, Itamar S Santos, Jose G Mill and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
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

13 authors at 5 institutions in 3 countries.

Isabela BensenorCenter for Clinical and Epidemiologic Research, University of São Paulo, São Paulo, Brazil.
Kallyandra PadilhaLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Isabella Ramos LimaLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Raul Dias SantosLipid Clinic, Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Gilles LambertInserm UMR 1188 DéTROI, Université La Réunion, Sainte Clotilde, France.
Stéphane Ramin-MangataInserm UMR 1188 DéTROI, Université La Réunion, Sainte Clotilde, France.
Marcio S BittencourtLipid Clinic, Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Alessandra C GoulartCenter for Clinical and Epidemiologic Research, University of São Paulo, São Paulo, Brazil.
Itamar S SantosCenter for Clinical and Epidemiologic Research, University of São Paulo, São Paulo, Brazil.
Jose G MillDepartment of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil.
Jose E KriegerLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Paulo A LotufoCenter for Clinical and Epidemiologic Research, University of São Paulo, São Paulo, Brazil.
Alexandre C PereiraLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Universidade de São Paulo · BRHospital São Paulo · BRInserm · FRUniversidade Federal do Espírito Santo · BRUniversity of Reunion Island · RE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological inhibition of PCSK9 (proprotein convertase subtilisin/kexin type 9) is an established therapeutic option to treat hypercholesterolemia, and plasma PCSK9 levels have been implicated in cardiovascular disease incidence. A number of genetic variants within the PCSK9 gene locus have been shown to modulate PCSK9 levels, but these only explain a very small percentage of the overall PCSK9 interindividual variation. Here we present data on the genetic association structure between PCSK9 levels and genom-wide genetic variation in a healthy sample from the general population. We performed a genome-wide association study of plasma PCSK9 levels in a sample of Brazilian individuals enrolled in the Estudo Longitudinal de Saude do Adulto cohort (

Indexed as

atherosclerosiscolocalization analysisgenetic variationgenome-wide association studyproprotein convertase subtilisin/kexin type 9

Identifiers

PMID34659352
PMCPMC8514075
OpenAlexW3203456995

What Socratic holds

Textmetadata
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 Socratic graph.