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- yes (61)
Is part of the Bibliography
- no (61)
Keywords
- TAVI (4)
- alirocumab (4)
- Aortic stenosis (3)
- Inflammation (3)
- acute coronary syndrome (3)
- Cardiovascular biology (2)
- MitraClip (2)
- biomarker (2)
- 16 segment AHA model (1)
- Acute coronary syndrome (1)
Institute
Hoffmann, Jedrzej ; Luxán, Guillermo ; Abplanalp, Wesley Tyler ; Glaser, Simone F. ; Rasper, Tina ; Fischer, Ariane ; Muhly-Reinholz, Marion ; Potente, Michael ; Aßmus, Birgit ; John, David ; Zeiher, Andreas M. ; Dimmeler, Stefanie
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.