Post-myocardial infarction heart failure dysregulates the bone vascular niche


  • J. Hoffmann
  • G. Luxán
  • W.T. Abplanalp
  • S.F. Glaser
  • T. Rasper
  • A. Fischer
  • M. Muhly-Reinholz
  • M. Potente
  • B. Assmus
  • D. John
  • A.M. Zeiher
  • S. Dimmeler


  • Nature Communications


  • Nat Commun 12 (1): 3964


  • 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.