ArticleJACC. Basic to translational science2025
Inhibition of Scarb1 on Endothelial Cells Attenuates Pressure Overload-Induced Heart Failure Progression.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Distinct Endothelial Phenotype Associates with Macrophage-Enriched Microenvironments in Triple-Negative Breast Cancer.Research square · 2026Article
- Capillary Endothelial Cells as Therapeutic Target in Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2025Article
- Heart failure-specific cardiac fibroblasts contribute to cardiac dysfunction via the MYC-CXCL1-CXCR2 axis.Nature cardiovascular research · 2025Article
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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