Post-myocardial infarction heart failure dysregulates the bone vascular niche

Jedrzej Hoffmann, Guillermo Luxán, Wesley Tyler Abplanalp, Simone-Franziska Glaser, Tina Rasper, Ariane Fischer, Marion Muhly-Reinholz, Michael Potente, Birgit Assmus, David John, Andreas Michael Zeiher and Stefanie Dimmeler ()
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Jedrzej Hoffmann: Center of Internal Medicine, Goethe University Frankfurt
Guillermo Luxán: German Center for Cardiovascular Research DZHK
Wesley Tyler Abplanalp: German Center for Cardiovascular Research DZHK
Simone-Franziska Glaser: German Center for Cardiovascular Research DZHK
Tina Rasper: Institute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University Frankfurt
Ariane Fischer: Institute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University Frankfurt
Marion Muhly-Reinholz: Institute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University Frankfurt
Michael Potente: Angiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research
Birgit Assmus: Center of Internal Medicine, Goethe University Frankfurt
David John: German Center for Cardiovascular Research DZHK
Andreas Michael Zeiher: Center of Internal Medicine, Goethe University Frankfurt
Stefanie Dimmeler: German Center for Cardiovascular Research DZHK

Nature Communications, 2021, vol. 12, issue 1, 1-11

Abstract: Abstract The 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.

Date: 2021
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DOI: 10.1038/s41467-021-24045-4

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