Heart to heart: grafting cardiosphere-derived cells augments cardiac self-repair by both myocytes and stem cells

Compared with highly regenerative potentially be exploited by the body itself namely that bone marrow cells likely organisms such as newts and zebrafish (Kikuchi & Poss, 2012), the capacity of mammalian adult heart tissue to undergo self-repair is insufficient to reconstitute the muscle lost in myocardial infarction, hindering functional recovery from heart attacks and from cell loss occurring in chronic heart failure (Mercola et al, 2011). The irreversibility of cell cycle exit in adult cardiomyocytes largely prevents the restoration of pump function via proliferation of pre-formed myocytes. However, overriding or inactivating tumour suppressor pocket proteins is one route to engineer persistent cycling in the adult heart (Mercola et al, 2011), and low levels of on-going myocyte generation have been demonstrated by fate-mapping inmice (Hsieh et al, 2007) and C dating in human heart tissue (Bergmann et al, 2009). Although quite limited, at least in healthy aging hearts, such turnover is conceptually important, as the underlying mechanism(s) could