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招募的巨细胞引起心房动

Maarten Hulsmans ^1,2, Maximilian J Schloss ^1,2, I-Hsiu Lee ^1,2

¹Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
²Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
³Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
⁴Department of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany.
⁵Department of Thoracic and Cardiovascular Surgery, University Hospital Wuerzburg, Wuerzburg, Germany.
⁶Department of Pathology, Center for Integrated Diagnostics, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
⁷Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
⁸Radcliffe Department of Medicine, NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.
⁹British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, UK.
¹⁰Institut del Cor Germans Trias i Pujol, CIBERCV, Badalona, Barcelona, Spain.
¹¹Department of Cardiology and Angiology, University of Giessen/DZHK, Partner Site Rhein-Main, Germany.
¹²Division of Cardiac Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
¹³Department of Surgery, Yale School of Medicine, New Haven, CT, USA.
¹⁴Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁵Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
¹⁶Department of Cardiac Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
¹⁷Leducq Foundation, Boston, MA, USA.
¹⁸Cardiovascular Disease Initiative, The Broad Institute of MIT and Harvard University, Cambridge, MA, USA.
¹⁹Department of Internal Medicine I, University Hospital Wuerzburg, Wuerzburg, Germany.

⁰Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Science (New York, N.Y.) +

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2023年七月13日

在PubMed上查看摘要

概括

免疫细胞,特别是SPP1+巨细胞,通过破坏心脏收缩来驱动心房动. 针对这些巨细胞提供了一种预防中风和心力衰竭的新疗法.

科学领域

心血管研究
免疫学
细胞生物学

背景情况

心房动会损害心房收缩,增加中风和心力衰竭的风险.
免疫和层细胞在AF病变中的作用尚不完全理解.

研究的目的

调查免疫和脑膜细胞对心房的贡献.
确定特定的细胞参与者和驱动AF的分子机制.

主要方法

人和小鼠心房的单细胞RNA测序.
开发一种结合高血压,肥胖和中枢反 (HOMER) 的小鼠模型.
基因操纵 (Ccr2淘汰,Spp1删除) 和细胞相互作用分析.

主要成果

单细胞转录组显示了人类和HOMER小鼠心房中的炎症单细胞和SPP1+巨细胞的扩张.
霍默小鼠表现出扩大,纤维化,容易发生心脏病的前庭,
抑制单细胞迁移 (Ccr2-/ -) 和删除Spp1 减少了HOMER小鼠的AF发生率.
SPP1被确定为一个关键的信号分子,它调解免疫细胞和树皮细胞之间的交叉对话,促进AF.

结论

SPP1+巨细胞是心房动的关键驱动因素.
向SPP1+巨细胞是一种潜在的AF免疫治疗策略.
了解免疫细胞的相互作用对于开发新型的AF治疗至关重要.