Circulation has retracted a 2012 study by a group of Harvard heart specialists over concerns of corrupt data, and the university is investigating. The group was led by Piero Anversa, a leading cardiologist, and Joseph Loscalzo — who will be familiar to readers of Circulation as the editor in chief of that journal. (Anversa’s also on the editorial board).
The paper was titled “Cardiomyogenesis in the aging and failing human heart,” and has been cited 30 times, according to Thomson Scientific’s Web of Knowledge. Here’s the abstract:
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 (14)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.
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.
According to the retraction statement:
For the article by Jan Kajstura, Marcello Rota, Donato Cappetta, Barbara Ogórek, Christian Arranto, Yingnan Bai, João Ferreira Martins, Sergio Signore, Fumihiro Sanada, Alex Matsuda, James Kostyla, Maria-Virginia Caballero, Claudia Fiorini, David A. D’Alessandro, Robert E. Michler, Federica del Monte, Toru Hosoda, Mark A. Perrella, Annarosa Leri, Bruce A. Buchholz, Joseph Loscalzo, and Piero Anversa (Cardiomyogenesis in the aging and failing human heart. Circulation. 2012;126:18691881; DOI: 10.1161/CIRCULATIONAHA.112.118380), an ongoing institutional review by Harvard Medical School and Brigham and Women’s Hospital has determined that the data are sufficiently compromised that a retraction is warranted.
The American Heart Association, therefore, retracts the article.
We’ve emailed Anversa for comment and will add to this post as we learn more.
One thing to note: Harvard probably isn’t the only institution looking at this matter. Per the paper:
This work was supported by NIH grants and by grant NCRR RR13461. This work was performed in part under the auspices of the U.S. Department of Energy by Lawrence Livermore National Laboratory under Contract DE-AC52-07NA27344.
Please see an update on this post.
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