{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Matsui M"],"funding":["American Heart Association","NICHD NIH HHS","NHLBI","NHLBI NIH HHS","NICHD"],"pagination":["e155569"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8983132"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(5)"],"pubmed_abstract":["Calcific aortic valve disease (CAVD) is heritable, as revealed by recent GWAS. While polymorphisms linked to increased expression of CACNA1C - encoding the CaV1.2 L-type voltage-gated Ca2+ channel - and increased Ca2+ signaling are associated with CAVD, whether increased Ca2+ influx through the druggable CaV1.2 causes CAVD is unknown. We confirmed the association between increased CaV1.2 expression and CAVD in surgically removed aortic valves from patients. We extended our studies with a transgenic mouse model that mimics increased CaV1.2 expression within aortic valve interstitial cells (VICs). In young mice maintained on normal chow, we observed dystrophic valve lesions that mimic changes found in presymptomatic CAVD and showed activation of chondrogenic and osteogenic transcriptional re"],"journal":["JCI insight"],"pubmed_title":["Increased Ca2+ influx through CaV1.2 drives aortic valve calcification."],"pmcid":["PMC8983132"],"funding_grant_id":["7POST33670699","R01 HD090132","R01 HL146149","R01HL151190,R01HL146149","R01HD090132","R01 HL151190"],"pubmed_authors":["Matsui M","Bouchareb R","Marx SO","Pitt GS","Storto M","Hussain Y","Gregg A"],"additional_accession":[]},"is_claimable":false,"name":"Increased Ca2+ influx through CaV1.2 drives aortic valve calcification.","description":"Calcific aortic valve disease (CAVD) is heritable, as revealed by recent GWAS. While polymorphisms linked to increased expression of CACNA1C - encoding the CaV1.2 L-type voltage-gated Ca2+ channel - and increased Ca2+ signaling are associated with CAVD, whether increased Ca2+ influx through the druggable CaV1.2 causes CAVD is unknown. We confirmed the association between increased CaV1.2 expression and CAVD in surgically removed aortic valves from patients. We extended our studies with a transgenic mouse model that mimics increased CaV1.2 expression within aortic valve interstitial cells (VICs). In young mice maintained on normal chow, we observed dystrophic valve lesions that mimic changes found in presymptomatic CAVD and showed activation of chondrogenic and osteogenic transcriptional re","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2026-05-31T13:01:13.596Z","creation":"2025-04-06T21:53:59.497Z"},"accession":"S-EPMC8983132","cross_references":{"pubmed":["35104251"],"doi":["10.1172/jci.insight.155569"]}}