TY - JOUR
T1 - Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy
AU - IMPC Consortium
AU - Genomics England Research Consortium
AU - Spielmann, Nadine
AU - Miller, Gregor
AU - Oprea, Tudor I.
AU - Hsu, Chih Wei
AU - Fobo, Gisela
AU - Frishman, Goar
AU - Montrone, Corinna
AU - Haseli Mashhadi, Hamed
AU - Mason, Jeremy
AU - Munoz Fuentes, Violeta
AU - Leuchtenberger, Stefanie
AU - Ruepp, Andreas
AU - Wagner, Matias
AU - Westphal, Dominik S.
AU - Wolf, Cordula
AU - Görlach, Agnes
AU - Sanz-Moreno, Adrián
AU - Cho, Yi Li
AU - Teperino, Raffaele
AU - Brandmaier, Stefan
AU - Sharma, Sapna
AU - Galter, Isabella Rikarda
AU - Östereicher, Manuela A.
AU - Zapf, Lilly
AU - Mayer-Kuckuk, Philipp
AU - Rozman, Jan
AU - Teboul, Lydia
AU - Bunton-Stasyshyn, Rosie K.A.
AU - Cater, Heather
AU - Stewart, Michelle
AU - Christou, Skevoulla
AU - Westerberg, Henrik
AU - Willett, Amelia M.
AU - Wotton, Janine M.
AU - Roper, Willson B.
AU - Christiansen, Audrey E.
AU - Ward, Christopher S.
AU - Heaney, Jason D.
AU - Reynolds, Corey L.
AU - Prochazka, Jan
AU - Bower, Lynette
AU - Clary, David
AU - Selloum, Mohammed
AU - Bou About, Ghina
AU - Wendling, Olivia
AU - Jacobs, Hugues
AU - Leblanc, Sophie
AU - Meziane, Hamid
AU - Sorg, Tania
AU - Wurst, Wolfgang
N1 - Publisher Copyright:
© 2022, The Author(s).
PY - 2022/2
Y1 - 2022/2
N2 - Clinical presentation of congenital heart disease is heterogeneous, making identification of the disease-causing genes and their genetic pathways and mechanisms of action challenging. By using in vivo electrocardiography, transthoracic echocardiography and microcomputed tomography imaging to screen 3,894 single-gene-null mouse lines for structural and functional cardiac abnormalities, here we identify 705 lines with cardiac arrhythmia, myocardial hypertrophy and/or ventricular dilation. Among these 705 genes, 486 have not been previously associated with cardiac dysfunction in humans, and some of them represent variants of unknown relevance (VUR). Mice with mutations in Casz1, Dnajc18, Pde4dip, Rnf38 or Tmem161b genes show developmental cardiac structural abnormalities, with their human orthologs being categorized as VUR. Using UK Biobank data, we validate the importance of the DNAJC18 gene for cardiac homeostasis by showing that its loss of function is associated with altered left ventricular systolic function. Our results identify hundreds of previously unappreciated genes with potential function in congenital heart disease and suggest causal function of five VUR in congenital heart disease.
AB - Clinical presentation of congenital heart disease is heterogeneous, making identification of the disease-causing genes and their genetic pathways and mechanisms of action challenging. By using in vivo electrocardiography, transthoracic echocardiography and microcomputed tomography imaging to screen 3,894 single-gene-null mouse lines for structural and functional cardiac abnormalities, here we identify 705 lines with cardiac arrhythmia, myocardial hypertrophy and/or ventricular dilation. Among these 705 genes, 486 have not been previously associated with cardiac dysfunction in humans, and some of them represent variants of unknown relevance (VUR). Mice with mutations in Casz1, Dnajc18, Pde4dip, Rnf38 or Tmem161b genes show developmental cardiac structural abnormalities, with their human orthologs being categorized as VUR. Using UK Biobank data, we validate the importance of the DNAJC18 gene for cardiac homeostasis by showing that its loss of function is associated with altered left ventricular systolic function. Our results identify hundreds of previously unappreciated genes with potential function in congenital heart disease and suggest causal function of five VUR in congenital heart disease.
UR - http://www.scopus.com/inward/record.url?scp=85141500188&partnerID=8YFLogxK
U2 - 10.1038/s44161-022-00018-8
DO - 10.1038/s44161-022-00018-8
M3 - Article
AN - SCOPUS:85141500188
SN - 2731-0590
VL - 1
SP - 157
EP - 173
JO - Nature Cardiovascular Research
JF - Nature Cardiovascular Research
IS - 2
ER -