抑制内皮细胞的Scarb1可减轻压力超载引起的心力衰竭进展。

IF 8.4 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

JACC: Basic to Translational Science Pub Date : 2025-07-07 DOI:10.1016/j.jacbts.2025.05.003

Toshiomi Katsuki, Dai Kusumoto, Yohei Akiba, Mai Kimura, Jin Komuro, Takahiro Nakamura, Hisayuki Hashimoto, Thukaa Kouka, Kazuhisa Sugai, Yoshinori Katsumata, Masaki Miyasaka, Yutaka Suzuki, Junko Kuramoto, Yoshiaki Kubota, Keiichi Fukuda, Shinsuke Yuasa, Masaki Ieda

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引用次数: 0

摘要

内皮细胞（EC）不适当的相互作用导致心力衰竭；然而，它们的确切机制仍然知之甚少。本研究在小鼠心力衰竭模型中使用单细胞rna测序分析了Scarb1介导的ec -成纤维细胞相互作用。内皮细胞表现出炎症和纤维化基因表达，scarb1介导的成纤维细胞-内皮细胞相互作用驱动疾病进展。ec特异性Scarb1敲除和系统性Scarb1抑制可减轻心力衰竭的进展。体外和空间组学分析证实了SCARB1在心力衰竭进展过程中在ECs和细胞-细胞相互作用中的作用。这些发现突出表明SCARB1是一个有希望的针对ec的干预治疗靶点。

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Inhibition of Scarb1 on Endothelial Cells Attenuates Pressure Overload-induced Heart Failure Progression.

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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来源期刊

JACC: Basic to Translational Science CARDIAC & CARDIOVASCULAR SYSTEMS-

CiteScore

14.20

自引率

1.00%

发文量

161

审稿时长

16 weeks

期刊介绍： JACC: Basic to Translational Science is an open access journal that is part of the renowned Journal of the American College of Cardiology (JACC). It focuses on advancing the field of Translational Cardiovascular Medicine and aims to accelerate the translation of new scientific discoveries into therapies that improve outcomes for patients with or at risk for Cardiovascular Disease. The journal covers thematic areas such as pre-clinical research, clinical trials, personalized medicine, novel drugs, devices, and biologics, proteomics, genomics, and metabolomics, as well as early phase clinical trial methodology.