Abstract
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. The present brief review highlights a few of these recent advances and provides a perspective for future clinical and experimental studies.
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