Abstract

Tissue injury elicits a regenerative response designed to restore its function through replacement of damaged cells. Such repair is thought to involve lineage-specific, tissue-specific progenitor cells that have been identified in most tissues, including the heart.1–3 The effectiveness of this repair ranges from minimal to complete, depending, among other factors, on the involved organ and the age of the individual in question, with certain organs such as the brain or the heart thought to have very low repair potential. Furthermore, little role has been ascribed to bone marrow–derived progenitors in adult tissue repair. Recent studies, however, have challenged both of these paradigms. The notion that the heart is a terminally differentiated organ without the capability of self-renewal has been challenged by the discovery of cardiac-specific progenitor cells residing in the myocardium.3 However, it is unclear how much functional effect such repair processes have and whether they can be effectively stimulated with pharmacological or biological therapies. Article p 3097 The beneficial effects observed after transplantation of various cell types into the myocardium in animal models of acute myocardial infarction (AMI)4 have led to the initiation of clinical studies even though the mechanism of these effects remains uncertain. The cell types tested in the setting of acute myocardial ischemia have ranged from unfractionated to different fractions of bone marrow–derived or peripheral blood mononuclear cells delivered by percutaneous intramyocardial or intracoronary injections.4 Essentially all studies have suggested some biological effectiveness, although in all cases, this conclusion is tempered by the uncontrolled nature and the small size of the trials. Nevertheless, the suggested benefits of cell therapy in AMI settings led Ince et al to perform the study reported in the current issue of Circulation .5 Instead of carrying out injections of one or another cell population, the authors …

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