A growing body of clinical and experimental evidence has led to the identification of nodal points in the pathways that drive the onset and progression of human cardiomyopathies. Studies of familial forms of human cardiomyopathy have documented that there are links between sarcomeric and cytoskeletal components, and onset of hypertrophic and dilated cardio-myopathy, respectively.
Studies of gene-targeted mice suggest that pathways that guide biomechanical signalling, myocyte survival, cardiac calcium cycling and the electrophysiological function of conduction system lineages may play critical roles in the onset of distinct phenotypes that arise in human forms of cardiomyopathy.
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The present brief review highlights a few of these recent advances and provides a perspective for future clinical and experimental studies. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In.
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Volume 3. Trib1 is a lipid- and myocardial infarction—associated gene that regulates hepatic lipogenesis and VLDL production in mice. Ralph Burkhardt, … , Jan L. Rader Ralph Burkhardt, … , Jan L.
View: Text PDF. Categories: Brief Report Genetics. View all copies of this ISBN edition:. Synopsis About this title Introducing a text oriented toward molecular cardiology that integrates all of the current knowledge in the field. Review : "A timely text that provides a comprehensive and up-to-date review of molecular biologic principles and their application to cardiovascular practice.
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Cellular and Molecular Pathobiology of Cardiovascular Disease
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