Genome-wide association studies highlight novel risk loci for septal defects and left-sided congenital heart defects.

Congenital heart disease Genetics Genome-wide association study Single nucleotide polymorphisms

Journal

BMC genomics
ISSN: 1471-2164
Titre abrégé: BMC Genomics
Pays: England
ID NLM: 100965258

Informations de publication

Date de publication:
07 Mar 2024
Historique:
received: 04 08 2023
accepted: 28 02 2024
medline: 8 3 2024
pubmed: 8 3 2024
entrez: 8 3 2024
Statut: epublish

Résumé

Congenital heart defects (CHD) are structural defects of the heart affecting approximately 1% of newborns. They exhibit low penetrance and non-Mendelian patterns of inheritance as varied and complex traits. While genetic factors are known to play an important role in the development of CHD, the specific genetics remain unknown for the majority of patients. To elucidate the underlying genetic risk, we performed a genome wide association study (GWAS) of CHDs in general and specific CHD subgroups using the FinnGen Release 10 (R10) (N > 393,000), followed by functional fine-mapping through eQTL and co-localization analyses using the GTEx database. We discovered three genome-wide significant loci associated with general CHD. Two of them were located in chromosome 17: 17q21.32 (rs2316327, intronic: LRRC37A2, Odds ratio (OR) [95% Confidence Interval (CI)] = 1.17[1.12-1.23], p = 1.5 × 10 Our results of general CHD and different CHD subcategories identified a complex risk locus on chromosome 17 near BAHCC1 and LRRC37A2, interacting with the genes WNT9B, WNT3 and MYL4, may constitute potential novel CHD risk associated loci, warranting future experimental tests to determine their role.

Sections du résumé

BACKGROUND BACKGROUND
Congenital heart defects (CHD) are structural defects of the heart affecting approximately 1% of newborns. They exhibit low penetrance and non-Mendelian patterns of inheritance as varied and complex traits. While genetic factors are known to play an important role in the development of CHD, the specific genetics remain unknown for the majority of patients. To elucidate the underlying genetic risk, we performed a genome wide association study (GWAS) of CHDs in general and specific CHD subgroups using the FinnGen Release 10 (R10) (N > 393,000), followed by functional fine-mapping through eQTL and co-localization analyses using the GTEx database.
RESULTS RESULTS
We discovered three genome-wide significant loci associated with general CHD. Two of them were located in chromosome 17: 17q21.32 (rs2316327, intronic: LRRC37A2, Odds ratio (OR) [95% Confidence Interval (CI)] = 1.17[1.12-1.23], p = 1.5 × 10
CONCLUSIONS CONCLUSIONS
Our results of general CHD and different CHD subcategories identified a complex risk locus on chromosome 17 near BAHCC1 and LRRC37A2, interacting with the genes WNT9B, WNT3 and MYL4, may constitute potential novel CHD risk associated loci, warranting future experimental tests to determine their role.

Identifiants

pubmed: 38454350
doi: 10.1186/s12864-024-10172-x
pii: 10.1186/s12864-024-10172-x
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

256

Informations de copyright

© 2024. The Author(s).

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Auteurs

Martin Broberg (M)

Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00014, Helsinki, Finland.
Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, 00014, Helsinki, Finland.

Minna Ampuja (M)

Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00014, Helsinki, Finland.

Samuel Jones (S)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, 00014, Helsinki, Finland.

Tiina Ojala (T)

Department of Pediatric Cardiology, New Children's Hospital, Pediatric Research Center, Helsinki University Hospital, 00029, Helsinki, Finland.

Otto Rahkonen (O)

Department of Pediatric Cardiology, New Children's Hospital, Pediatric Research Center, Helsinki University Hospital, 00029, Helsinki, Finland.

Riikka Kivelä (R)

Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00014, Helsinki, Finland.
Wihuri Research Institute, 00290, Helsinki, Finland.
Faculty of Sport and Health Sciences, University of Jyväskylä, 40014, Jyväskylä, Finland.

James Priest (J)

School of Medicine, Stanford University, Stanford University, Stanford, CA, 94305, USA.

Aarno Palotie (A)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, 00014, Helsinki, Finland.

Hanna M Ollila (HM)

Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki, 00014, Helsinki, Finland.
Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, 02142, USA.
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.

Emmi Helle (E)

Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00014, Helsinki, Finland. emmi.helle@helsinki.fi.
Department of Pediatric Cardiology, New Children's Hospital, Pediatric Research Center, Helsinki University Hospital, 00029, Helsinki, Finland. emmi.helle@helsinki.fi.
, Haartmaninkatu 8, Helsinki, 00014, Finland. emmi.helle@helsinki.fi.
Population Health Unit, Finnish Institute for Health and Welfare, Helsinki, 00271, Finland. emmi.helle@helsinki.fi.

Classifications MeSH