Eliciting Heart Regeneration through Cardiomyocyte Division

European Coordinator:
  • Elly TANAKA, Research Institute of Molecular Pathology, Vienna (Austria)
North American Coordinator:
  • Kenneth POSS, Duke University Medical Center, Durham (USA)
  • Nenad BURSAC, Duke University, Durham (USA)
  • Robert GRAHAM, Richard HARVEY, Victor Chang Cardiac Research Institute, Sydney (Australia)
  • Ahsan HUSAIN, Emory University, Atlanta (USA)
  • Bernhard KUHN, Children’s Hospital of Pittsburg (USA)
  • Didier STAINIER, Max Planck Institute for Heart and Lung Research, Bad Nauheim (Germany)
  • Eldad TZAHOR, Weizmann Institute of Science, Rehovot (Israel)


The human heart shows limited natural muscle regeneration in response to myocardial infarction. Instead of re-growing functional heart tissue, the human heart, in response to a heart attack, produces a non-function scar.   There is currently no therapy that successfully regenerates heart tissue, and this despite more than a decade of stem cell research that initially appeared to be very promising in this regard. One new promising line of research focuses on expanding the heart’s limited ability to produce new muscle cells. This network enlists an interdisciplinary team of biologists, clinicians and engineers with the following objectives: 1) Discover factors that stimulate cardiomyocyte (cardiac muscle cell) division using in vivo models of embryonic and postnatal heart development, natural heart regeneration in zebrafish and mice, engineered human cardiac muscle constructs, and the classical models of tissue regeneration in salamanders; 2) Elucidate the mechanism to discover how we might be able to influence mammalian cardiac repair. 3) Develop pre-clinical mammalian models of regenerative therapy through the delivery of cardiomyocyte mitogens and the engineering of cardiac tissue patches from stem cell-derived cardiomyocytes. These approaches will define regulatory mechanisms for heart regeneration and derive new regenerative approaches to cardiovascular disease.