Evidence map›Paper›PMID 37000167›Full record

ArticleeLife2023

The potential of integrating human and mouse discovery platforms to advance our understanding of cardiometabolic diseases.

Aaron W Jurrjens, Marcus M Seldin, Corey Giles, Peter J Meikle, Brian G Drew, Anna C Calkin

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 6 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

6 authors at 2 institutions in 2 countries.

Aaron W JurrjensBaker Heart and Diabetes Institute, Melbourne, Australia.ORCID 0000-0003-2349-4122
Marcus M SeldinDepartment of Biological Chemistry and Center for Epigenetics and Metabolism, University of California, Irvine, Irvine, United States.ORCID 0000-0001-8026-4759
Corey GilesBaker Heart and Diabetes Institute, Melbourne, Australia.ORCID 0000-0002-6050-1259
Peter J MeikleBaker Heart and Diabetes Institute, Melbourne, Australia.ORCID 0000-0002-2593-4665
Brian G Drew *Baker Heart and Diabetes Institute, Melbourne, Australia.ORCID 0000-0002-7839-9467
Anna C Calkin *Baker Heart and Diabetes Institute, Melbourne, Australia.ORCID 0000-0002-9861-0602
Baker Heart and Diabetes Institute · AUUniversity of California, Irvine · US

Funding

Integrative approaches to dissection of endocrine communicationDP1DK130640 · NIDDK · UNIVERSITY OF CALIFORNIA-IRVINE · PI SELDIN, MARCUS MICHAEL · 2021 to 2025
$3.2M
NIDDK NIH HHS DP1 DK130640NIH HHS DP1 DK130640
6 · The paper itself

Abstract

Cardiometabolic diseases encompass a range of interrelated conditions that arise from underlying metabolic perturbations precipitated by genetic, environmental, and lifestyle factors. While obesity, dyslipidaemia, smoking, and insulin resistance are major risk factors for cardiometabolic diseases, individuals still present in the absence of such traditional risk factors, making it difficult to determine those at greatest risk of disease. Thus, it is crucial to elucidate the genetic, environmental, and molecular underpinnings to better understand, diagnose, and treat cardiometabolic diseases. Much of this information can be garnered using systems genetics, which takes population-based approaches to investigate how genetic variance contributes to complex traits. Despite the important advances made by human genome-wide association studies (GWAS) in this space, corroboration of these findings has been hampered by limitations including the inability to control environmental influence, limited access to pertinent metabolic tissues, and often, poor classification of diseases or phenotypes. A complementary approach to human GWAS is the utilisation of model systems such as genetically diverse mouse panels to study natural genetic and phenotypic variation in a controlled environment. Here, we review mouse genetic reference panels and the opportunities they provide for the study of cardiometabolic diseases and related traits. We discuss how the post-GWAS era has prompted a shift in focus from discovery of novel genetic variants to understanding gene function. Finally, we highlight key advantages and challenges of integrating complementary genetic and multi-omics data from human and mouse populations to advance biological discovery.

Indexed as

Cardiovascular DiseasesGenome-Wide Association StudyAnimalsGenetic Predisposition to DiseaseHumansMiceObesityPhenotypeRisk Factorsatherosclerosiscardiometabolic diseasecomputational biologycoronary artery diseasegenetic mappinggenetic reference panelsgeneticsgenome-wide association studiesgenomicsHybrid Mouse Diversity Panelmulti-omicsnon-alcoholic fatty liver diseasesystems biologysystems genetics

Identifiers

PMID37000167
PMCPMC10065800
OpenAlexW4362475491

What OpenQuestion 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 OpenQuestion graph.