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We are analyzing https://www.biorxiv.org/content/10.1101/2025.02.20.639228v1.

Title:
Cell type-specific epigenetic regulatory circuitry of coronary artery disease loci | bioRxiv
Description:
Coronary artery disease (CAD) is the leading cause of death worldwide. Recently, hundreds of genomic loci have been shown to increase CAD risk, however, the molecular mechanisms underlying signals from CAD risk loci remain largely unclear. We sought to pinpoint the candidate causal coding and non-coding genes of CAD risk loci in a cell type-specific fashion. We integrated the latest statistics of CAD genetics from over one million individuals with epigenetic data from 45 relevant cell types to identify genes whose regulation is affected by CAD-associated single nucleotide variants (SNVs) via epigenetic mechanisms. Applying two statistical approaches, we identified 1,580 genes likely involved in CAD, about half of which have not been associated with the disease so far. Enrichment analysis and phenome-wide association studies linked the novel candidate genes to disease-specific pathways and CAD risk factors, corroborating their disease relevance. We showed that CAD-SNVs are enriched to regulate gene expression by affecting the binding of transcription factors (TFs) with cellular specificity. Of all the candidate genes, 23.5% represented non-coding RNAs (ncRNA), which likewise showed strong cell type specificity. We conducted a proof-of-concept biological validation for the novel CAD ncRNA gene IQCH-AS1 . CRISPR/Cas9-based gene knockout of IQCH-AS1 , in a human preadipocyte strain, resulted in reduced preadipocyte proliferation, less adipocyte lipid accumulation, and atherogenic cytokine profile. The cellular data are in line with the reduction of IQCH-AS1 in adipose tissues of CAD patients and the negative impact of risk alleles on its expression, suggesting IQCH-AS1 to be protective for CAD. Our study not only pinpoints CAD candidate genes in a cell type-specific fashion but also spotlights the roles of the understudied ncRNA genes in CAD genetics. ### Competing Interest Statement The authors have declared no competing interest. All data generated or analysed during this study are included in this published article (and its supplementary information files), except for the raw STARNET which was made accessible by members of the STARNET project.
Website Age:
12 years and 2 months (reg. 2013-04-08).

Matching Content Categories {📚}

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Content Management System {📝}

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Website use Drupal 7 (http://drupal.org).

Traffic Estimate {📈}

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💥 Very Strong Traffic: 200k - 500k visitors per month


Based on our best estimate, this website will receive around 261,717 visitors per month in the current month.

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How Does Biorxiv.org Make Money? {💸}

We can't see how the site brings in money.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Biorxiv.org could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

cad, biology, genes, cell, risk, disease, loci, candidate, genetics, data, iqchas, medrxiv, subject, reviews, clinical, preprint, typespecific, epigenetic, gene, ncrna, biorxiv, university, trials, epidemiology, search, results, coronary, artery, profile, pdf, molecular, mechanisms, noncoding, fashion, factors, showed, expression, cellular, specificity, preadipocyte, study, competing, interest, authors, supplementary, information, starnet, made, project, copyright,

Topics {✒️}

crispr/cas9-based gene knockout epidemiology subject categories cell type-specific fashion clinical trials supplementary information files biorxiv subject category microbiology epidemiology papers reviews disease-specific pathways cad genetics author/funder cad risk loci keyword advanced search atherogenic cytokine profile health-related information regulate gene expression ranjan kumar maji fatemeh behjati ardakani single nucleotide variants concept biological validation human preadipocyte strain reduced preadipocyte proliferation adipocyte lipid accumulation suggesting iqch-as1 generous financial support chan zuckerberg initiative imperial college london vrije universiteit amsterdam articles animal behavior increase cad risk epigenetic data cad risk factors understudied ncrna genes candidate causal coding competing interest statement genetics context cellular data data availability data generated epigenetic mechanisms genomic loci disease relevance cellular specificity iqch-as1 shuangyue li risk alleles candidate genes competing interest

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Mail Servers:

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