ABSTRACT
Cardiac scarring and persistent muscle cell loss is the hallmark of myocardial infarction in humans. This biological limitation is found, too, with experimental myocardial infarction in other mammals, of less pressing clinical need-an inbuilt restriction contrasting with the exuberant restorative, regenerative growth that enables the total replacement of a limb, tail, or even heart in certain lower species1,2-‘lower’ being in this respect a sorely misleading designation. Quite recently, and with uncanny speed, the notion of cell implantation as a means to promote cardiac repair has moved from an esoteric laboratory phenomenon to a dramatic and closely watched series of clinical trials on the world stage, involving skeletal muscle as a cardiac surrogate,3 and progenitor/stem cells from bone marrow and the circulation as the agents of therapeutic angiogenesis and perhaps even as cardiac precursors.4-8 While some questions get posed with regularity (what cells to use, and how to deliver them), others are being asked more rarely (why does grafting work, and should a patient’s own-autologous-cells always be preferred to allogeneic ones?), and some are asked hardly at all (where and how do the endogenous adult cardiac progenitor cells arise?). The interventions now in play are remarkable for their therapeutic promise, their biological complexity, and the likelihood that defective stem cell function will be among the next therapeutic horizons.
