Evidence map›Paper›PMID 39141130›Full record

ArticleDiabetologia2024

Genetic relations between type 1 diabetes, coronary artery disease and leukocyte counts.

Jolade Adebekun, Ajay Nadig, Priscilla Saarah, Samira Asgari, Linda Kachuri, David A Alagpulinsa

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Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

3 citing papers in PubMed.

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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.

Jolade AdebekunYale Center for Molecular and Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Ajay NadigProgram in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Priscilla SaarahYale Center for Molecular and Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA.
Samira AsgariInstitute for Genomic Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Linda KachuriDepartment of Epidemiology and Population Health, Stanford University School of Medicine, Stanford, CA, USA.
David A AlagpulinsaYale Center for Molecular and Systems Metabolism, Yale University School of Medicine, New Haven, CT, USA. david.alagpulinsa@yale.edu.ORCID http://orcid.org/0000-0002-8737-4907

Funding

Medical Scientist Training ProgramT32GM144273 · NIGMS · HARVARD MEDICAL SCHOOL · PI David Shumway Jones, Jacqueline A. Lees · 2022 to 2026
$14.7M
Identifying genetic and sociodemographic determinants of susceptibility to infectious diseases in diverse population groupsR21MD019104 · NIMHD · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ASGARI, SAMIRA · 2023 to 2024
$444k
Juvenile Diabetes Research Foundation International 2-SRA-2022-1276-S-BNIGMS NIH HHS T32 GM144273NIMHD NIH HHS R21 MD019104
6 · The paper itself

Abstract

aims/hypothesisType 1 diabetes is associated with excess coronary artery disease (CAD) risk even when known cardiovascular risk factors are accounted for. Genetic perturbation of haematopoiesis that alters leukocyte production is a novel independent modifier of CAD risk. We examined whether there are shared genetic determinants and causal relationships between type 1 diabetes, CAD and leukocyte counts.

methodsGenome-wide association study summary statistics were used to perform pairwise linkage disequilibrium score regression and heritability estimation from summary statistics (ρ-HESS) to respectively estimate the genome-wide and local genetic correlations, and two-sample Mendelian randomisation to estimate the causal relationships between leukocyte counts (335,855 healthy individuals), type 1 diabetes (18,942 cases, 501,638 control individuals) and CAD (122,733 cases, 424,528 control individuals). A latent causal variable (LCV) model was performed to estimate the genetic causality proportion of the genetic correlation between type 1 diabetes and CAD.

resultsThere was significant genome-wide genetic correlation (r CONCLUSIONS/

interpretationThis study sheds light on shared genetic mechanisms underlying type 1 diabetes and CAD, which may contribute to their co-occurrence through regulation of gene expression and leukocyte counts and identifies cellular and molecular targets for further investigation for disease prediction and potential drug discovery.

Indexed as

Coronary Artery DiseaseDiabetes Mellitus, Type 1Genome-Wide Association StudyFemaleGenetic Predisposition to DiseaseHumansLeukocyte CountLinkage DisequilibriumMaleMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsCoronary artery diseaseExpression quantitative lociGenetic correlationGenetic riskHaematopoiesisLeukocyte countsMendelian randomisationType 1 diabetes

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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.