Cellular and molecular drivers of cardiac fibrosis and remodelling in health and disease

European Coordinator:
  • Norbert HUBNER, Max-Delbrück Center for Molecular Medicine, Berlin (Germany)
North American Coordinator:
  • Jonathan G. SEIDMAN, Harvard Medical School, Boston (USA)
  • Stefan BLANKENBERG, University Heart Center, Hamburg, (Germany)
  • Stuart COOK, Imperial College, London, (UK)
  • Sylvia EVANS, University of California San Diego, La Jolla, CA (USA)
  • Jean Philipp JUNKER, Max Delbruck Center for Molecular Medicine, Berlin (Germany)
  • David MERRYMAN, Vanderbilt University, Nashville (USA)
  • Christine SEIDMAN, Brigham & Women’s Hospital, Boston, MA (USA)


While much is known about cardiac myocytes, relatively less is known about non-myocytes, which make up approximately half of cardiac cells. These non-myocytes are involved in the heart’s response to injury, which often takes the form of tissue fibrosis, which can cause damage to the heart, including heart failure and deadly arrhythmias. Non-myocytes are activated in many common cardiac disorders, including acquired remodelling secondary to hypertension, ischemic heart failure, and valve disease. Little is know about how non-myocyte cells become activated, and indeed it is not even clear which cells are involved in pathological processes of fibrosis, or whether some populations of cells arrive from outside of the heart. This Leducq network will use sophisticated new technologies to examine the different non-myocyte cell populations in normal and diseased hearts, with an eye toward understanding the signalling processes that regulate cardiac non-myocyte growth. This new knowledge will be exploited, using human cohorts, to identify biomarkers that improve diagnosis and assess progression of maladaptive remodelling that promote human heart failure and adverse cardiovascular outcomes.