{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(10)"],"submitter":["Katsuki T"],"funding":["Takeda Science Foundation","Japan Agency for Medical Research and Development","Bayer","MSD"],"pubmed_abstract":["Inappropriate endothelial cell (EC) interactions contribute to heart failure; however, their precise mechanisms remain poorly understood. This study investigated EC-fibroblast interactions mediated by Scarb1 using single-cell RNA-sequencing analysis in a mouse heart failure model. ECs exhibited inflammatory and fibrotic gene expression, with Scarb1-mediated fibroblast-EC interactions driving disease progression. EC-specific Scarb1 knockout and systemic SCARB1 inhibition attenuated heart failure progression. In vitro and spatial omics analyses confirmed the role of SCARB1 in ECs and cell-cell interaction during heart failure progression. These findings highlight SCARB1 as a promising therapeutic target for EC-focused interventions."],"journal":["JACC. Basic to translational science"],"pagination":["101308"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12665495"],"repository":["biostudies-literature"],"pubmed_title":["Inhibition of Scarb1 on Endothelial Cells Attenuates Pressure Overload-Induced Heart Failure Progression."],"pmcid":["PMC12665495"],"pubmed_authors":["Kuramoto J","Fukuda K","Komuro J","Katsuki T","Kubota Y","Ieda M","Miyasaka M","Kimura M","Kusumoto D","Akiba Y","Suzuki Y","Yuasa S","Nakamura T","Kouka T","Sugai K","Katsumata Y","Hashimoto H"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of Scarb1 on Endothelial Cells Attenuates Pressure Overload-Induced Heart Failure Progression.","description":"Inappropriate endothelial cell (EC) interactions contribute to heart failure; however, their precise mechanisms remain poorly understood. This study investigated EC-fibroblast interactions mediated by Scarb1 using single-cell RNA-sequencing analysis in a mouse heart failure model. ECs exhibited inflammatory and fibrotic gene expression, with Scarb1-mediated fibroblast-EC interactions driving disease progression. EC-specific Scarb1 knockout and systemic SCARB1 inhibition attenuated heart failure progression. In vitro and spatial omics analyses confirmed the role of SCARB1 in ECs and cell-cell interaction during heart failure progression. These findings highlight SCARB1 as a promising therapeutic target for EC-focused interventions.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-06T15:02:17.269Z","creation":"2026-06-01T03:10:37.553Z"},"accession":"S-EPMC12665495","cross_references":{"pubmed":["40772900"],"doi":["10.1016/j.jacbts.2025.05.003"]}}