{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mallaredy V"],"funding":["NHLBI NIH HHS"],"pagination":["280-297"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11223950"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["135(2)"],"pubmed_abstract":["<h4>Background</h4>Heart failure (HF) is one of the leading causes of mortality worldwide. Extracellular vesicles, including small extracellular vesicles or exosomes, and their molecular cargo are known to modulate cell-to-cell communication during multiple cardiac diseases. However, the role of systemic extracellular vesicle biogenesis inhibition in HF models is not well documented and remains unclear.<h4>Methods</h4>We investigated the role of circulating exosomes during cardiac dysfunction and remodeling in a mouse transverse aortic constriction (TAC) model of HF. Importantly, we investigate the efficacy of tipifarnib, a recently identified exosome biogenesis inhibitor that targets the critical proteins (Rab27a [Ras associated binding protein 27a], nSMase2 [neutral sphingomyelinase 2], "],"journal":["Circulation research"],"pubmed_title":["Tipifarnib Reduces Extracellular Vesicles and Protects From Heart Failure."],"pmcid":["PMC11223950"],"funding_grant_id":["P01 HL147841","R01 HL169405","R01 HL143892","P01 HL134608","R01 HL091983"],"pubmed_authors":["Joladarashi D","Magadum A","Koch WJ","Ibetti J","Garikipati VNS","Cheng Z","Cimini M","Benedict C","Truongcao M","Mallaredy V","Roy R","Thej C","Gonzalez C","Kishore R"],"additional_accession":[]},"is_claimable":false,"name":"Tipifarnib Reduces Extracellular Vesicles and Protects From Heart Failure.","description":"<h4>Background</h4>Heart failure (HF) is one of the leading causes of mortality worldwide. Extracellular vesicles, including small extracellular vesicles or exosomes, and their molecular cargo are known to modulate cell-to-cell communication during multiple cardiac diseases. However, the role of systemic extracellular vesicle biogenesis inhibition in HF models is not well documented and remains unclear.<h4>Methods</h4>We investigated the role of circulating exosomes during cardiac dysfunction and remodeling in a mouse transverse aortic constriction (TAC) model of HF. Importantly, we investigate the efficacy of tipifarnib, a recently identified exosome biogenesis inhibitor that targets the critical proteins (Rab27a [Ras associated binding protein 27a], nSMase2 [neutral sphingomyelinase 2], ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-02T08:44:32.322Z","creation":"2026-04-16T03:12:46.98Z"},"accession":"S-EPMC11223950","cross_references":{"pubmed":["38847080"],"doi":["10.1161/circresaha.123.324110","10.1161/CIRCRESAHA.123.324110"]}}