{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mushtaq I"],"funding":["Taipei Municipal Wan-Fang Hospital","National Science and Technology Council"],"pagination":["110084"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11179076"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(6)"],"pubmed_abstract":["The mutated SCN5A gene encoding defective Nav1.5 protein causes arrhythmic ailments and is associated with enhanced cardiac fibrosis. This study investigated whether SCN5A mutation directly affects cardiac fibroblasts and explored how defective SCN5A relates to cardiac fibrosis. SCN5A knockdown (SCN5AKD) human cardiac fibroblasts (HCF) had higher collagen, α-SMA, and fibronectin expressions. Micro-RNA deep sequencing and qPCR analysis revealed the downregulation of miR-452-5p and bioinformatic analysis divulged maladaptive upregulation of transforming growth factor β (TGF-β) signaling in SCN5AKD HCF. Luciferase reporter assays validated miR-452-5p targets SMAD4 in SCN5AKD HCF. Moreover, miR-452-5p mimic transfection in SCN5AKD HCF or AAV9-mediated miR-452-5p delivery in isoproterenol-induc"],"journal":["iScience"],"pubmed_title":["MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts."],"pmcid":["PMC11179076"],"funding_grant_id":["113-wf-eva-12","108-2314-B-038-116","112-2314-B-038-068-MY2","111-wf-f-7"],"pubmed_authors":["Mushtaq I","Kao YH","Chen YC","Chen YJ","Hsieh TH"],"additional_accession":[]},"is_claimable":false,"name":"MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.","description":"The mutated SCN5A gene encoding defective Nav1.5 protein causes arrhythmic ailments and is associated with enhanced cardiac fibrosis. This study investigated whether SCN5A mutation directly affects cardiac fibroblasts and explored how defective SCN5A relates to cardiac fibrosis. SCN5A knockdown (SCN5AKD) human cardiac fibroblasts (HCF) had higher collagen, α-SMA, and fibronectin expressions. Micro-RNA deep sequencing and qPCR analysis revealed the downregulation of miR-452-5p and bioinformatic analysis divulged maladaptive upregulation of transforming growth factor β (TGF-β) signaling in SCN5AKD HCF. Luciferase reporter assays validated miR-452-5p targets SMAD4 in SCN5AKD HCF. Moreover, miR-452-5p mimic transfection in SCN5AKD HCF or AAV9-mediated miR-452-5p delivery in isoproterenol-induc","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-06-03T06:44:00.694Z","creation":"2025-04-19T15:42:30.735Z"},"accession":"S-EPMC11179076","cross_references":{"pubmed":["38883840"],"doi":["10.1016/j.isci.2024.110084"]}}