TY - JOUR
T1 - Cardiomyogenesis in the aging and failing human heart
AU - Kajstura, Jan
AU - Rota, Marcello
AU - Cappetta, Donato
AU - Ogórek, Barbara
AU - Arranto, Christian
AU - Bai, Yingnan
AU - Ferreira-Martins, João
AU - Signore, Sergio
AU - Sanada, Fumihiro
AU - Matsuda, Alex
AU - Kostyla, James
AU - Caballero, Maria Virginia
AU - Fiorini, Claudia
AU - Dalessandro, David A.
AU - Michler, Robert E.
AU - Del Monte, Federica
AU - Hosoda, Toru
AU - Perrella, Mark A.
AU - Leri, Annarosa
AU - Buchholz, Bruce A.
AU - Loscalzo, Joseph
AU - Anversa, Piero
PY - 2012/10/9
Y1 - 2012/10/9
N2 - Background-Two opposite views of cardiac growth are currently held; one views the heart as a static organ characterized by a large number of cardiomyocytes that are present at birth and live as long as the organism, and the other views the heart a highly plastic organ in which the myocyte compartment is restored several times during the course of life. Methods and Results-The average age of cardiomyocytes, vascular endothelial cells (ECs), and fibroblasts and their turnover rates were measured by retrospective C birth dating of cells in 19 normal hearts 2 to 78 years of age and in 17 explanted failing hearts 22 to 70 years of age. We report that the human heart is characterized by a significant turnover of ventricular myocytes, ECs, and fibroblasts, physiologically and pathologically. Myocyte, EC, and fibroblast renewal is very high shortly after birth, decreases during postnatal maturation, remains relatively constant in the adult organ, and increases dramatically with age. From 20 to 78 years of age, the adult human heart entirely replaces its myocyte, EC, and fibroblast compartment 8, 6, and 8 times, respectively. Myocyte, EC, and fibroblast regeneration is further enhanced with chronic heart failure. Conclusions-The human heart is a highly dynamic organ that retains a remarkable degree of plasticity throughout life and in the presence of chronic heart failure. However, the ability to regenerate cardiomyocytes, vascular ECs, and fibroblasts cannot prevent the manifestations of myocardial aging or oppose the negative effects of ischemic and idiopathic dilated cardiomyopathy.
AB - Background-Two opposite views of cardiac growth are currently held; one views the heart as a static organ characterized by a large number of cardiomyocytes that are present at birth and live as long as the organism, and the other views the heart a highly plastic organ in which the myocyte compartment is restored several times during the course of life. Methods and Results-The average age of cardiomyocytes, vascular endothelial cells (ECs), and fibroblasts and their turnover rates were measured by retrospective C birth dating of cells in 19 normal hearts 2 to 78 years of age and in 17 explanted failing hearts 22 to 70 years of age. We report that the human heart is characterized by a significant turnover of ventricular myocytes, ECs, and fibroblasts, physiologically and pathologically. Myocyte, EC, and fibroblast renewal is very high shortly after birth, decreases during postnatal maturation, remains relatively constant in the adult organ, and increases dramatically with age. From 20 to 78 years of age, the adult human heart entirely replaces its myocyte, EC, and fibroblast compartment 8, 6, and 8 times, respectively. Myocyte, EC, and fibroblast regeneration is further enhanced with chronic heart failure. Conclusions-The human heart is a highly dynamic organ that retains a remarkable degree of plasticity throughout life and in the presence of chronic heart failure. However, the ability to regenerate cardiomyocytes, vascular ECs, and fibroblasts cannot prevent the manifestations of myocardial aging or oppose the negative effects of ischemic and idiopathic dilated cardiomyopathy.
KW - carbon radioisotopes
KW - cell proliferation
KW - cytokinesis
KW - myocytes, cardiac
KW - radiometric dating
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U2 - 10.1161/CIRCULATIONAHA.112.118380
DO - 10.1161/CIRCULATIONAHA.112.118380
M3 - Article
C2 - 22955965
AN - SCOPUS:84867241732
SN - 0009-7322
VL - 126
SP - 1869
EP - 1881
JO - Circulation
JF - Circulation
IS - 15
ER -