STAT3 expression is reduced in cardiac pericytes in HFpEF and its loss reduces cellular adhesion and induces pericyte senescence

IF 3.5 4区生物学 Q1 Biochemistry, Genetics and Molecular Biology

FEBS Letters Pub Date : 2025-05-01 DOI:10.1002/1873-3468.70057

Leah Rebecca Vanicek, Ariane Fischer, Mariano Ruz Jurado, Anita Tamiato, Tara Procida-Kowalski, Jochen Wilhelm, Dennis Hecker, Maximilian Merten, Felicitas Escher, Badder Kattih, Valentina Puntmann, David John, Marcel H. Schulz, Eike Nagel, Stefanie Dimmeler, Guillermo Luxán

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引用次数: 0

Abstract

Heart failure with preserved ejection fraction (HFpEF) accounts for half of heart failure cases and is characterised by reduced pericyte coverage. While the contributions of other cardiac cell types to HFpEF are well-studied, the role of pericytes remains less understood. Using murine single-nucleus RNA-sequencing to study cardiac pericytes in HFpEF, we identified reduced STAT3 expression as a hallmark of HFpEF pericytes. Mechanistic studies in vitro revealed that STAT3 deletion induces cellular senescence and impairs pericyte adhesion, recapitulating HFpEF-like characteristics. These findings suggest that STAT3 is crucial for maintaining pericyte homeostasis and highlight its reduction as a potential driver of pericyte loss, a defining feature of HFpEF.

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HFpEF患者心脏周细胞中STAT3的表达降低，STAT3的缺失降低了细胞粘附，诱导周细胞衰老。

保留射血分数（HFpEF）的心力衰竭占心力衰竭病例的一半，其特征是周细胞覆盖减少。虽然其他心脏细胞类型对HFpEF的贡献已经得到了很好的研究，但周细胞的作用仍然知之甚少。利用小鼠单核rna测序研究HFpEF的心脏周细胞，我们发现STAT3表达降低是HFpEF周细胞的标志。体外机制研究表明，STAT3缺失诱导细胞衰老，损害周细胞粘附，重现hfpef样特征。这些发现表明STAT3对于维持周细胞稳态至关重要，并强调其减少是周细胞损失的潜在驱动因素，这是HFpEF的一个决定性特征。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

FEBS Letters 生物-生化与分子生物学

CiteScore

7.00

自引率

2.90%

发文量

303

审稿时长

1.0 months

期刊介绍： FEBS Letters is one of the world''s leading journals in molecular biology and is renowned both for its quality of content and speed of production. Bringing together the most important developments in the molecular biosciences, FEBS Letters provides an international forum for Minireviews, Research Letters and Hypotheses that merit urgent publication.