Abstract

The letter by Bergmann and collaborators1 questions our comments2 regarding their work on 14C birth dating of human cardiomyocytes with aging.3 Three points are made in an attempt to challenge the issues we have raised, which cast serious doubts on the validity of their data on myocyte turnover with physiological aging: (1) appropriateness of the myocardial samples examined; (2) specificity of the protocol used for the isolation of myocyte nuclei; and (3) correct interpretation of the 14C measurements. As acknowledged in their letter, 6 of the 12 hearts studied, that is, 50% of the cases, had overt myocardial pathology. Surprisingly, samples collected from a patient who died of acute myocardial infarction were considered representative of normal cardiac aging. Additionally, no histological analysis was performed in the 6 “nonpathological” hearts; gross examination at autopsy was deemed to be sufficient to define the structural integrity of the myocardium. Specific clinical, anatomic, and histological criteria have to be met for the inclusion of human hearts in studies of physiological aging (Table).4,5 The approach used by Bergmann and collaborators is far from any sensible standard needed to determine the biology of human cardiac aging. View this table: Table. Inclusion Criteria for the Analysis of Physiological Myocardial Aging The authors defend the findings reported in Science 3 by citing the article that subsequently appeared in Experimental Cell Research .6 We have been criticized in the letter for ignoring this hastily published report. Our reasons for not quoting this second report must be discussed. In this work, a series of images illustrating different degrees of nuclear troponin staining have been obtained with a variety of antigen retrieval methods. These findings have been interpreted as unequivocal documentation of the expression of troponin I in myocyte nuclei, independent from the age of …

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