Tachycardia can be prevented by engrafting embryonic cardiomyocytes into mice. A protein resident at 'gap junctions', connexin 43, is also identified as being important for this protection. Expression of this protein in skeletal myoblasts achieves similar levels of protection. These results suggest a new approach to cell-based therapy for cardiac dysfunction.
- Wilhelm Roell
- Thorsten Lewalter
- Bernd K. Fleischmann
