{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Borges KS"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NIGMS NIH HHS"],"pubmed_abstract":["The steroid hormone aldosterone, produced by the zona glomerulosa (zG) of the adrenal gland, is a master regulator of plasma electrolytes and blood pressure. While aldosterone control by the renin-angiotensin system is well understood, other key regulatory factors have remained elusive. Here, we replicated a prior association between a non-coding variant in <i>WNT2B</i> and an increased risk of primary aldosteronism, a prevalent and debilitating disease caused by excessive aldosterone production. We further show that in both mice and humans, WNT2B is expressed in the mesenchymal capsule surrounding the adrenal cortex, in close proximity to the zG. Global loss of <i>Wnt2b</i> in the mouse results in a dysmorphic and hypocellular zG, with impaired aldosterone production. Similarly, humans ha"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2024.08.23.609423"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11370552"],"repository":["biostudies-literature"],"pubmed_title":["Non-canonical Wnt signaling triggered by WNT2B drives adrenal aldosterone production."],"pmcid":["PMC11370552"],"funding_grant_id":["K12 DK133995","R01 GM122920","R35 GM153357","K08 DK120871","R01 DK062027","R01 HL155834","R01 DK123694"],"pubmed_authors":["Seth A","Barrett PQ","Azova S","Guagliardo NA","Magalhaes TA","Hammer GD","Borges KS","Little DW","Berber M","Lerario AM","Carlone DL","Ribeiro C","Turcu AF","Hirschhorn JN","Mohan DR","Breault DT","Salic A","Rainey W","O'Connell AE","Basham KJ","Dumontet T","Lapensee C"],"additional_accession":[]},"is_claimable":false,"name":"Non-canonical Wnt signaling triggered by WNT2B drives adrenal aldosterone production.","description":"The steroid hormone aldosterone, produced by the zona glomerulosa (zG) of the adrenal gland, is a master regulator of plasma electrolytes and blood pressure. While aldosterone control by the renin-angiotensin system is well understood, other key regulatory factors have remained elusive. Here, we replicated a prior association between a non-coding variant in <i>WNT2B</i> and an increased risk of primary aldosteronism, a prevalent and debilitating disease caused by excessive aldosterone production. We further show that in both mice and humans, WNT2B is expressed in the mesenchymal capsule surrounding the adrenal cortex, in close proximity to the zG. Global loss of <i>Wnt2b</i> in the mouse results in a dysmorphic and hypocellular zG, with impaired aldosterone production. Similarly, humans ha","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-07-05T03:14:41.703Z","creation":"2025-04-06T14:25:34.752Z"},"accession":"S-EPMC11370552","cross_references":{"pubmed":["39229119"],"doi":["10.1101/2024.08.23.609423"]}}