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  Post-myocardial infarction heart failure dysregulates the bone vascular niche

Hoffmann, J., Luxan, G., Abplanalp, W. T., Glaser, S.-F., Rasper, T., Fischer, A., et al. (2021). Post-myocardial infarction heart failure dysregulates the bone vascular niche. NATURE COMMUNICATIONS, 12(1): 3964. doi:10.1038/s41467-021-24045-4.

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Genre: Journal Article

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 Creators:
Hoffmann, Jedrzej, Author
Luxan, Guillermo, Author
Abplanalp, Wesley Tyler, Author
Glaser, Simone-Franziska, Author
Rasper, Tina, Author
Fischer, Ariane, Author
Muhly-Reinholz, Marion, Author
Potente, Michael1, Author              
Assmus, Birgit, Author
John, David, Author
Zeiher, Andreas Michael, Author
Dimmeler, Stefanie, Author
Affiliations:
1Angiogenesis & Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591701              

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Free keywords: CELL; ANGIOGENESIS; MYCScience & Technology - Other Topics;
 Abstract: Hematopoiesis influences the progression of cardiovascular disease, yet the influence of cardiovascular disease on the bone vasculature is unknown. Hoffmann, Luxan, Abplanalp et al. describe the response of the bone cell composition to myocardial infarction and provide a rationale for using anti-inflammatory therapies to prevent the deterioration of the bone vascular niche 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-1 beta 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.

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Language(s): eng - English
 Dates: 2021-06-25
 Publication Status: Published online
 Pages: 11
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000687320200024
DOI: 10.1038/s41467-021-24045-4
PMID: 34172720
 Degree: -

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Title: NATURE COMMUNICATIONS
Source Genre: Journal
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Publ. Info: HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY : NATURE PORTFOLIO
Pages: - Volume / Issue: 12 (1) Sequence Number: 3964 Start / End Page: - Identifier: ISSN: 2041-1723