Evidence map›Paper›PMID 40341583›Full record

ArticleNature communications2025

Human genetic variation determines 24-hour rhythmic gene expression and disease risk.

Ying Chen, Panpan Liu, Aniko Sabo, Dongyin Guan

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Ying ChenDivision of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Panpan LiuDivision of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Aniko SaboHuman Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA.
Dongyin GuanDivision of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. dongyin.guan@bcm.edu.ORCID http://orcid.org/0000-0002-2641-3095

Funding

The Human Genome Sequencing CenterU54HG003273 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI GIBBS, RICHARD A · 2004 to 2015
$341.3M
Genomic Architecture of Common Disease in Diverse Populations: WGS of Ongoing Hemorrhagic Stroke Study SupplementUM1HG008898 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI GIBBS, RICHARD A · 2016 to 2020
$77.0M
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Suzanne AW Fuqua · 2007 to 2026
$73.9M
Tissue Analysis & Molecular Imaging CoreP30DK056338 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Hashem B El-Serag · 2001 to 2026
$28.3M
GENETICS OF CHILDHOOD OBESITYR01DK059264 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BUTTE, NANCY F · 2000 to 2004
$2.7M
Obesity and Diabetes Familial Risk in Hispanic ChildrenR01DK080457 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BUTTE, NANCY F. · 2009 to 2012
$2.5M
Comprehensive SNP Discovery in SLC2A9. A Candidate Gene for Uric Acid NephropathyR01DK092238 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI VORUGANTI, VENKATA SAROJA · 2012 to 2015
$1.3M
3D Circadian Enhancer-Promoter Interactions Mediated by ESRRG in NAFLD-to-HCC ProgressionR37CA296577 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Dongyin Guan · 2025 to 2026
$1.1M
Defining the role of non-clock genes in circadian physiology and pathophysiologyK01DK125602 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GUAN, DONGYIN · 2020 to 2023
$562k
Cancer Prevention and Research Institute of Texas (Cancer Prevention Research Institute of Texas) RR210029NCI NIH HHS P30 CA125123NCI NIH HHS R37 CA296577NHGRI NIH HHS U54 HG003273NHGRI NIH HHS UM1 HG008898NIDDK NIH HHS K01 DK125602NIDDK NIH HHS P30 DK056338NIDDK NIH HHS R01 DK059264NIDDK NIH HHS R01 DK080457NIDDK NIH HHS R01 DK092238U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) K01-DK125602V Foundation for Cancer Research (V Foundation) V2022-026
6 · The paper itself

Abstract

24-hour biological rhythms are essential to maintain physiological homeostasis. Disruption of these rhythms increases the risks of multiple diseases. Biological rhythms are known to have a genetic basis formed by core clock genes, but how individual genetic variation shapes the oscillating transcriptome and contributes to human chronophysiology and disease risk is largely unknown. Here, we mapped interactions between temporal gene expression and genotype to identify quantitative trait loci (QTLs) contributing to rhythmic gene expression. These newly identified QTLs were termed as rhythmic QTLs (rhyQTLs), which determine previously unappreciated rhythmic genes in human subpopulations with specific genotypes. Functionally, rhyQTLs and their associated rhythmic genes contribute extensively to essential chronophysiological processes, including bile acid and lipid metabolism. The identification of rhyQTLs sheds light on the genetic mechanisms of gene rhythmicity, offers mechanistic insights into variations in human disease risk, and enables precision chronotherapeutic approaches for patients.

Indexed as

Circadian RhythmGene Expression RegulationGenetic Predisposition to DiseaseGenetic VariationQuantitative Trait LociFemaleGenotypeHumansLipid MetabolismMalePolymorphism, Single NucleotideTranscriptome

Identifiers

PMID40341583
PMCPMC12062405

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.