Resident fibroblast lineages mediate pressure overload–induced cardiac fibrosis

Activation and accumulation of cardiac fibroblasts, which result in excessive extracellular matrix deposition and consequent mechanical stiffness, myocyte uncoupling, and ischemia, are key contributors to heart failure progression. Recently, endothelial-to-mesenchymal transition (EndoMT) and the recruitment of circulating hematopoietic progenitors to the heart have been reported to generate substantial numbers of cardiac fibroblasts in response to pressure overload-induced injury; therefore, these processes are widely considered to be promising therapeutic targets. Here, using multiple independent murine Cre lines and a collagen1a1-GFP fusion reporter, which specifically labels fibroblasts, we found that…

• AH
  American Heart Association

  Awards: HL106968, HL066100, P30 NS047101
• NI
  National Institutes of Health

  Awards: HL119967, NS047101, HL106968, P30 NS047101
• UO
  University of California, San Diego

  Awards: P30 NS047101, NS047101
• NH
  National Heart, Lung, and Blood Institute

  Award: HL106968