| First Author | Hoffmann J | Year | 2021 |
| Journal | Nat Commun | Volume | 12 |
| Issue | 1 | Pages | 3964 |
| PubMed ID | 34172720 | Mgi Jnum | J:372374 |
| Mgi Id | MGI:6725563 | Doi | 10.1038/s41467-021-24045-4 |
| Citation | Hoffmann J, et al. (2021) Post-myocardial infarction heart failure dysregulates the bone vascular niche. Nat Commun 12(1):3964 |
| abstractText | 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-1beta 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. |
