Mapping the cardiac vascular niche in heart failure

Fabian Peisker, Maurice Halder, James Nagai, Susanne Ziegler, Nadine Kaesler, Konrad Hoeft, Ronghui Li, Eric M. J. Bindels, Christoph Kuppe, Julia Moellmann, Michael Lehrke, Christian Stoppe, Michael T. Schaub, Rebekka K. Schneider, Ivan Costa and Rafael Kramann ()
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Fabian Peisker: RWTH Aachen University Medical Faculty
Maurice Halder: RWTH Aachen University Medical Faculty
James Nagai: RWTH Aachen University Hospital
Susanne Ziegler: RWTH Aachen University Medical Faculty
Nadine Kaesler: RWTH Aachen University Medical Faculty
Konrad Hoeft: RWTH Aachen University Medical Faculty
Ronghui Li: RWTH Aachen University Hospital
Eric M. J. Bindels: Erasmus MC Cancer Institute
Christoph Kuppe: RWTH Aachen University Medical Faculty
Julia Moellmann: RWTH Aachen University Hospital
Michael Lehrke: RWTH Aachen University Hospital
Christian Stoppe: University Hospital Wuerzburg
Michael T. Schaub: RWTH Aachen University
Rebekka K. Schneider: RWTH Aachen University Hospital
Ivan Costa: RWTH Aachen University Hospital
Rafael Kramann: RWTH Aachen University Medical Faculty

Nature Communications, 2022, vol. 13, issue 1, 1-20

Abstract: 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.

Date: 2022
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DOI: 10.1038/s41467-022-30682-0

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