Key result
The myocardium demonstrates significant biochemical plasticity through protein isoform switches, such as myosin heavy chain transitions, in response to developmental, hormonal, and hemodynamic stimuli.
This review provides foundational insights into the molecular basis of cardiac performance, highlighting how the heart adapts to stress through contractile protein isoform switching.
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May inform understanding of cardiac adaptation; leaves open whether isoform switching can be therapeutically targeted.
Although the physiological properties of the myocardium and their dynamic character have been the focus of intense re- search during the past three decades, the biochemical and mo- lecular correlates underlying cardiac performance for the most part remain poorly understood.The central role of the myo- cardium in the maintenance of the cardiac output notwith- standing, until very recently the prevailing view of the heart was that of a biochemically very static organ.Therefore, it did not seem either particularly interesting or suitable to address major questions of cellular and molecular biology affecting normal and pathological states.As a consequence, the impact of the newly developed techniques of recombinant DNA and genetic manipulation in transgenic animals on the under- standing of cardiac cellular and molecular biology has been less significant than on other fields of biomedical sciences.With few exceptions, the power of these new techniques and approaches is just beginning to be felt in the field of cardiovas- cular biology.This state of affairs is more surprising given the biomedical importance of the cardiovascular system in general and the myocardium in particular, as well as the large number of investigators dedicated to its study.This situation is due, at least in part, to the characteristics of the myocardium that, until recently, have made this organ a less than ideal model system for a molecular and genetic approach.Due to the essential role ofthe myocardium in the survival of the organism, most of the genetic mutations that signifi- cantly affect its development and/or function are likely to be lethal.This feature explains the very small number of muta- tions described so far affecting the myocardium either in human or animal models.This is in contrast with the large number of mutations affecting blood cells, the endocrine sys- tem, and metabolic pathways, among others.The existence of these mutations has provided the port of entry for the molecu- lar dissection ofthese systems.In addition to the unavailability of mutations, the difficulty in obtaining repeated samples of the myocardium that are suitable for biochemical and molecu- lar analysis from the same animal has also slowed progress.Furthermore, the existence of well-characterized cell lines that can be grown in homogeneous populations and mutated at will are an almost essential requirement for the exploitation of
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Nadal-Ginard et al. (1989) conducted a review in Cardiac performance and myocardial plasticity. The myocardium demonstrates significant biochemical plasticity through protein isoform switches, such as myosin heavy chain transitions, in response to developmental, hormonal, and hemodynamic stimuli.
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