{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yao Q"],"funding":["NHLBI NIH HHS"],"pagination":["1410862"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11458440"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["<h4>Background</h4>Human Aortic valve interstitial cells (AVICs) from calcific aortic valve disease (CAVD)-affected valves exhibit elevated fibrocalcific activity although the underlying mechanism remains incompletely understood. This study aimed to identify endogenous factors that promote aortic valve fibrocalcification.<h4>Methods and results</h4>Proteomic analysis found increased cathepsin D levels in AVICs from CAVD-affected valves compared to AVICs from normal valves, and this finding was validated by immunoblotting. ELISA assay identified exacerbated release of cathepsin D by AVICs of diseased valves. Recombinant human cathepsin D upregulated the expression of runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), collagen I and collagen IV in human AVICs, resulting"],"journal":["Frontiers in cardiovascular medicine"],"pubmed_title":["Cathepsin D elevates the fibrocalcific activity in human aortic valve cells through the ERK1/2-Sox9 pathway."],"pmcid":["PMC11458440"],"funding_grant_id":["R01 HL121776"],"pubmed_authors":["Zhai Y","Ao L","The E","Fullerton DA","Yao Q","Nedumaran B","Meng X"],"additional_accession":[]},"is_claimable":false,"name":"Cathepsin D elevates the fibrocalcific activity in human aortic valve cells through the ERK1/2-Sox9 pathway.","description":"<h4>Background</h4>Human Aortic valve interstitial cells (AVICs) from calcific aortic valve disease (CAVD)-affected valves exhibit elevated fibrocalcific activity although the underlying mechanism remains incompletely understood. This study aimed to identify endogenous factors that promote aortic valve fibrocalcification.<h4>Methods and results</h4>Proteomic analysis found increased cathepsin D levels in AVICs from CAVD-affected valves compared to AVICs from normal valves, and this finding was validated by immunoblotting. ELISA assay identified exacerbated release of cathepsin D by AVICs of diseased valves. Recombinant human cathepsin D upregulated the expression of runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), collagen I and collagen IV in human AVICs, resulting","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2026-07-14T19:44:00.14Z","creation":"2025-04-03T23:48:47.531Z"},"accession":"S-EPMC11458440","cross_references":{"pubmed":["39380629"],"doi":["10.3389/fcvm.2024.1410862"]}}