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绘制心力衰竭中心血管壁龛图谱。

Mapping the cardiac vascular niche in heart failure.

机构信息

Institute of Experimental Medicine and Systems Biology, RWTH Aachen University Medical Faculty, Aachen, Germany.

Institute for Computational Genomics, RWTH Aachen University Hospital, Aachen, Germany.

出版信息

Nat Commun. 2022 May 31;13(1):3027. doi: 10.1038/s41467-022-30682-0.

Abstract

The cardiac vascular and perivascular niche are of major importance in homeostasis and during disease, but we lack a complete understanding of its cellular heterogeneity and alteration in response to injury as a major driver of heart failure. Using combined genetic fate tracing with confocal imaging and single-cell RNA sequencing of this niche in homeostasis and during heart failure, we unravel cell type specific transcriptomic changes in fibroblast, endothelial, pericyte and vascular smooth muscle cell subtypes. We characterize a specific fibroblast subpopulation that exists during homeostasis, acquires Thbs4 expression and expands after injury driving cardiac fibrosis, and identify the transcription factor TEAD1 as a regulator of fibroblast activation. Endothelial cells display a proliferative response after injury, which is not sustained in later remodeling, together with transcriptional changes related to hypoxia, angiogenesis, and migration. Collectively, our data provides an extensive resource of transcriptomic changes in the vascular niche in hypertrophic cardiac remodeling.

摘要

心脏血管和血管周隙在维持内环境稳定和疾病发生过程中具有重要作用,但我们对其细胞异质性以及损伤反应中的改变缺乏全面的了解,后者是心力衰竭的主要驱动因素。通过对该血管周隙在维持内环境稳定和心力衰竭过程中的遗传命运追踪,并结合共聚焦成像和单细胞 RNA 测序,我们揭示了成纤维细胞、内皮细胞、周细胞和血管平滑肌细胞亚型中特定的转录组变化。我们描述了一个在维持内环境稳定时存在的特定成纤维细胞亚群,该亚群在损伤后获得 Thbs4 表达并扩增,从而驱动心脏纤维化,并确定转录因子 TEAD1 是成纤维细胞激活的调节因子。内皮细胞在损伤后表现出增殖反应,但在后期重塑过程中不能持续,同时还伴有与缺氧、血管生成和迁移相关的转录变化。总的来说,我们的数据为肥厚性心脏重塑中血管周隙的转录组变化提供了广泛的资源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd0f/9156759/1e0c1ed8dbc3/41467_2022_30682_Fig1_HTML.jpg

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