The adult heart has the capacity to generate new myocytes that are markedly enhanced in
acute and chronic heart failure of ischemic and non-ischemic origin. In addition, a pool of blood trafficking
progenitor cells able to sense myocardial damage may home to the sites of injury participating
to cardiac repair. This new view of myocardial biology leads to an expanding long-term research and therapeutic goals for
cardioprotection. A fundamental concept to be analyzed is whether cardiac diseases are influenced by changes in the
properties of tissue specific and circulating progenitors. Loss of self-renewal capacity, impaired growth or increased susceptibility
to death may lead to a reduction of progenitors and leave myocardial damage unrepaired. Cardiac progenitors
generate all myocardial cell lineages, thus impairment in their growth is expected to be critically involved in the structural
and functional modifications of the heart. The fact that, in addition to well known effects of anthracyclines, also new
drugs that target molecular pathways implicated in cell death and growth can be cardiotoxic further supports our hypothesis.
Understanding the role of resident and extracardiac progenitors in the pathogenesis of cardiomyopathies of different
etiology will provide not only a better comprehension of cardiac homeostasis but will also open new avenues for therapeutic
interventions. The progress toward effective myocardial regeneration based on exploiting the self-renewal potential of
the myocardium and the systemic pool of cardiogenic cells should advance the likelihood of efficient cardioprotection and
restoration of cardiac function.
Keywords: Cardiac progenitors, cardioprotection, cardiotoxiciy, ischemic cardiomyopathy, regenerative medicine, stem cells.
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