Evidence map›Paper›PMID 40176577›Full record

ArticleDisease models & mechanisms2025

Identifying links between cardiovascular disease and insomnia by modeling genes from a pleiotropic locus.

Farah Abou Daya, Torrey Mandigo, Lily Ober, Dev Patel, Matthew Maher, Suraj Math, Cynthia Tchio, James A Walker, Richa Saxena, Girish C Melkani

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease models & mechanisms, 2025. 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.

  1. Article
  2. Article
  3. 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

10 authors.

Farah Abou DayaDepartment of Pathology, Division of Molecular and Cellular Pathology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Torrey MandigoCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Lily OberDepartment of Pathology, Division of Molecular and Cellular Pathology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Dev PatelDepartment of Pathology, Division of Molecular and Cellular Pathology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Matthew MaherCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Suraj MathCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Cynthia TchioCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
James A WalkerCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Richa SaxenaCenter for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Girish C MelkaniDepartment of Pathology, Division of Molecular and Cellular Pathology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.ORCID 0000-0003-0353-4633

Funding

American Heart Association 23PRE1020631NHLBI Division of Intramural Research HL146751NHLBI NIH HHS R01 HL146751University of Alabama at Birmingham 3123226
6 · The paper itself

Abstract

Insomnia symptoms double the risk of cardiovascular disease (CVD), yet shared genetic pathways remain unclear. Genome-wide association studies identified a genetic locus (near ATP5G1, UBE2Z, SNF8, IGF2BP1 and GIP) linked to insomnia and CVD. We used Drosophila models to perform tissue-specific RNA interference knockdowns of four conserved orthologs (ATPsynC, lsn, Bruce and Imp) in neurons and the heart. Neuronal-specific knockdown of ATPsynC, Imp and lsn impaired sleep quantity and quality. In contrast, cardiac knockdown of ATPsynC and lsn reduced cardiac function and lifespan, with lsn knockdown also causing cardiac dilation and myofibrillar disorganization. Cross-tissue effects were evident: neuronal Imp knockdown compromised cardiac function, whereas cardiac ATPsynC and lsn knockdown increased sleep fragmentation and inflammation (marked by Upd3 elevation in the heart or head). Overexpression of Upd3 in neurons impaired cardiac function, and its overexpression in the heart disrupted sleep. Our findings reveal conserved genes mediating tissue-specific and cross-tissue interactions between sleep and cardiac function, providing novel insights into the genetic mechanisms linking insomnia and CVD through inflammation.

Indexed as

Cardiovascular DiseasesDrosophila melanogasterGenes, InsectGenetic PleiotropyModels, GeneticSleep Initiation and Maintenance DisordersAnimalsDisease Models, AnimalDrosophila ProteinsGene Knockdown TechniquesGenome-Wide Association StudyMyocardiumNeuronsOrgan SpecificityRNA InterferenceSleepDrosophila ProteinsCardiovascular diseaseDrosophila modelGenetic lociGWASInflammationInsomniars4643373 locus

Identifiers

PMID40176577
PMCPMC12140649

What Socratic holds

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LicenceCC BY
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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 Socratic graph.