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(Hypertension. 2007;49:427.)
© 2007 American Heart Association, Inc.
Editorial Commentaries |
From the Johns Hopkins University School of Medicine, Baltimore, Md.
Correspondence to Oscar H. Cingolani, Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, 600 N Wolfe St/Carnegie 568, Baltimore, MD 21287. E-mail ocingol1@jhmi.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The heart responds to sustained pressure overload with hypertrophy. Although at first glance this seems to be an adaptive mechanism by which the heart battles against increased workload, there is evidence that these "compensatory changes," even early in the game, are different from the benign, truly adaptive response that occurs, for example, in athletes.1 In this group, hypertrophy is characterized by "physiological" myocyte growth and usually does not carry a poor prognosis. On the other hand, in hypertrophy associated with cardiovascular diseases, such as hypertension or aortic stenosis, increased expression of noncontractile proteins, such as collagen, as well as fetal isoforms of contractile proteins, take place, resulting in fibrosis, diastolic dysfunction, and, subsequently, heart failure. Therefore, differentiating the adaptive or "good" hypertrophy from the maladaptive or "bad" hypertrophy and their different pathways seems to be appropriate. Over the past decades, scientists have been studying left ventricular hypertrophy and its many intracellular mechanisms, trying to better understand the cellular changes that lead to pressure-activated hypertrophy and subsequent heart failure. It appears that some of these changes might be compensatory and some others, detrimental.1
The Wnt signaling pathways play key roles in the differentiation, proliferation, death, and function of cells and, as a result, are involved in critical developmental, growth, and homeostatic processes. The Wnts are a family of genes/proteins. They have been linked to Alzheimers disease, aortic valve calcification, cancer, and diseases affecting bone.2 Control of the Wnt pathways is modulated by a number of proteins that either interact with the
Related Article:
Hypertension 2007 49: 473-480.
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