Evidence map›Paper›PMID 37333408›Full record

ArticlebioRxiv : the preprint server for biology2023

Shared and distinct pathways and networks genetically linked to coronary artery disease between human and mouse.

Zeyneb Kurt, Jenny Cheng, Caden N McQuillen, Zara Saleem, Neil Hsu, Nuoya Jiang, Rio Barrere-Cain, Calvin Pan, Oscar Franzen, Simon Koplev and 5 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Zeyneb KurtDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Jenny ChengDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Caden N McQuillenDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Zara SaleemDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Neil HsuDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Nuoya JiangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Rio Barrere-CainDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Calvin PanDepartment of Medicine, Division of Cardiology, University of California, Los Angeles, 650 Charles E Young Drive South, Los Angeles, CA 90095-1679, USA.
Oscar FranzenDepartment of Genetics & Genomic Sciences, Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, US.
Simon KoplevDepartment of Genetics & Genomic Sciences, Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, US.
Susanna WangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Johan BjorkegrenDepartment of Genetics & Genomic Sciences, Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029-6574, US.
Aldons J LusisDepartment of Medicine, Division of Cardiology, University of California, Los Angeles, 650 Charles E Young Drive South, Los Angeles, CA 90095-1679, USA.
Montgomery BlencoweDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.
Xia YangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Drive East, Los Angeles, CA 90095, USA.

Funding

Systems Genetics Dissection of Non-alcoholic SteatohepatitisR01DK117850 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Aldons Jake Lusis · 2019 to 2026
$4.6M
Multimodal genetic regulatory architecture of coronary artery diseaseR01HL148239 · NHLBI · UNIVERSITY OF VIRGINIA · PI Clint L Miller · 2019 to 2026
$4.2M
Integrative genomic and functional genomic studies to connect variant to function for CAD GWAS lociR01HL168174 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Wei Li, EDOARDO MARCORA · 2023 to 2026
$3.1M
Systems genetics approach to inflammatory mechanisms in atherosclerosisR01HL147883 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2019 to 2022
$3.0M
Understanding the Molecular Mechanisms of Fibromuscular DysplasiaR01HL148167 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KADIAN-DODOV, DANIELLA, KOVACIC, JASON CIRIL · 2020 to 2023
$2.8M
Systems Genetics of Vascular Smooth Muscle PhenotypesR01HL166428 · NHLBI · UNIVERSITY OF VIRGINIA · PI Mete Civelek · 2023 to 2026
$2.4M
Functional genomics investigation of pleiotropic vascular disease lociR01HL164577 · NHLBI · UNIVERSITY OF VIRGINIA · PI MILLER, CLINT L · 2022 to 2025
$2.3M
NHLBI NIH HHS R01 HL147883NHLBI NIH HHS R01 HL148167NHLBI NIH HHS R01 HL148239NHLBI NIH HHS R01 HL164577NHLBI NIH HHS R01 HL166428NHLBI NIH HHS R01 HL168174NIDDK NIH HHS R01 DK117850
6 · The paper itself

Abstract

Mouse models have been used extensively to study human coronary artery disease (CAD) or atherosclerosis and to test therapeutic targets. However, whether mouse and human share similar genetic factors and pathogenic mechanisms of atherosclerosis has not been thoroughly investigated in a data-driven manner. We conducted a cross-species comparison study to better understand atherosclerosis pathogenesis between species by leveraging multiomics data. Specifically, we compared genetically driven and thus CAD-causal gene networks and pathways, by using human GWAS of CAD from the CARDIoGRAMplusC4D consortium and mouse GWAS of atherosclerosis from the Hybrid Mouse Diversity Panel (HMDP) followed by integration with functional multiomics human (STARNET and GTEx) and mouse (HMDP) databases. We found that mouse and human shared >75% of CAD causal pathways. Based on network topology, we then predicted key regulatory genes for both the shared pathways and species-specific pathways, which were further validated through the use of single cell data and the latest CAD GWAS. In sum, our results should serve as a much-needed guidance for which human CAD-causal pathways can or cannot be further evaluated for novel CAD therapies using mouse models.

Indexed as

AtherosclerosisCoronary Artery DiseaseCross-species ComparisonGene NetworksGWASHumanLiverMouseMultiomicsVascular Tissues

Identifiers

PMID37333408
PMCPMC10274918

What OpenQuestion holds

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LicenceCC BY-ND
Read underepoch 390

Registered trials

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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.