Dissemin is shutting down on January 1st, 2025

Published in

Nature Research, Nature Communications, 1(12), 2021

DOI: 10.1038/s41467-021-24045-4

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Post-myocardial infarction heart failure dysregulates the bone vascular niche

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

AbstractThe regulation of bone vasculature by chronic diseases, such as heart failure is unknown. Here, we describe the effects of myocardial infarction and post-infarction heart failure on the bone vascular cell composition. We demonstrate an age-independent loss of type H endothelium in heart failure after myocardial infarction in both mice and humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium, showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1β production partially prevented the post-myocardial infarction loss of type H vasculature in mice. These results provide a rationale for using anti-inflammatory therapies to prevent or reverse the deterioration of bone vascular function in ischemic heart disease.