Evidence map›Paper›PMID 25870159›Full record

ReviewJournal of molecular and cellular cardiology2015

Genome-wide association studies of late-onset cardiovascular disease.

J Gustav Smith, Christopher Newton-Cheh

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

Review in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
7.2field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 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

2 authors at 2 institutions in 2 countries.

J Gustav SmithCenter for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA; Department of Cardiology, Clinical Sciences, Lund University and Skåne University Hospital, Lund, Sweden. Electronic address: gustav.smith@med.lu.se.
Christopher Newton-ChehCenter for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA. Electronic address: cnewtoncheh@mgh.harvard.edu.
Center for Human Genetics · USSkåne University Hospital · SE

Funding

Genetics of Cardiotoxic Drug Response to Psychiatric TherapyR01HL124262 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NEWTON-CHEH, CHRISTOPHER HOLMES, PERLIS, ROY H. · 2015 to 2018
$2.7M
Physiologic Profiling of sGC Genetic VariantsR01HL113933 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NEWTON-CHEH, CHRISTOPHER HOLMES · 2013 to 2016
$2.3M
NHLBI NIH HHS R01 HL113933NHLBI NIH HHS R01HL113933NHLBI NIH HHS R01 HL124262NHLBI NIH HHS R01HL124262
6 · The paper itself

Abstract

Human genetics is a powerful tool for discovering causal mediators of human disease and physiology. Cardiovascular diseases with late onset in the lifecourse have historically not been considered genetic diseases, but in recent years the contribution of a heritable factor has been established. More importantly, over the last decade genome-wide association studies (GWASs) have identified many loci associated with late-onset cardiovascular diseases including coronary artery disease, carotid artery disease, ischemic stroke, aortic aneurysm, peripheral vascular disease, atrial fibrillation, valvular disease and correlates of vascular and myocardial function. Here we review findings from GWASs considered statistically robust with regard to multiple testing (p<5×10(-8)) for late-onset cardiovascular diseases and traits. Although for only a handful of the 92 genetic loci described here have the mechanisms underlying disease association been established, new and previously unsuspected pathways have been implicated for several conditions. Examples include a role for NO signaling in myocardial repolarization and sudden cardiac death and a role for the protein sortilin in lipid metabolism and coronary artery disease. Genetic loci with multiple trait associations have also provided novel biological insights. For example, of the 46 genetic loci associated with coronary artery disease, only 16 are also associated with conventional risk factors for cardiovascular disease whereas the remaining two thirds may reflect novel pathways. Much work remains to functionally characterize genetic loci and for clinical utility, but accruing insights into the biological basis of cardiovascular aging in human populations promise to point to novel therapeutic and preventive strategies. This article is part of a Special Issue entitled 'SI:CV Aging'.

Indexed as

Genetic LociGenetic Predisposition to DiseaseAge of OnsetAnimalsArrhythmias, CardiacArteriesCoronary Artery DiseaseGenome, HumanGenome-Wide Association StudyHeartHumansMyocardial InfarctionPhenotypeSarcomeresStrokeAgingCardiovascular diseaseGenome-wide association study

Identifiers

PMID25870159
PMCPMC4459905
OpenAlexW2059116451

What OpenQuestion holds

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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.