Cardiac Regeneration and Aging
This chapter discusses inability of the mammalian heart to regenerate parenchymal cells, that is, decrease in the number of ventricular myocytes which results in aging and cardiac diseases. The effects of age and pathological states on the number of tissue-specific cell types are similar in organs with high- or low-turnover cell rates. In myocardium, adaptation to stress involves an increased replicative response that does not maintain tissue homeostasis, since cell death exceeds cell division (Kempermann et al., 2004; Urbanek et al., 2005). The behavior of the heart, therefore, corresponds to a model of tissue growth essentially common to all organs in the organism. Chronological age represents an objective useful parameter to compare the function of organs in age-matched individuals and evaluate whether heart failure correlates with biological age. With this approach, the properties of cardiac stem/progenitor cells can be compared and properly analyzed. Therefore, to establish whether biological aging can induce an aging cardiomyopathy independent of other causes, patients have been carefully selected and all known causes of heart failure— hypertension, ischemic heart disease, diabetes, systemic disorders, drug or alcohol abuse and myocarditis—have been excluded (Chimenti et al., 2003). However, the definition of an aging myopathy is further complicated by the necessity to distinguish the senescent failing heart from idiopathic dilated cardiomyopathy.