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• W2141195909 abstract "See related articles, pages 81–87 and 125–132 The cytoskeleton of cardiac myocytes is a complex network of many interacting protein filaments and associated proteins with multiple functions: it forms structures responsible for maintaining cell shape and contractile filament registration, structural integrity, internal transport and cell division, and scaffolding for several putative signaling cascades.1 The tight coupling between the extracellular matrix and components of the cytoskeleton at the cell membrane suggests that, in addition to transmitting contractile forces generated by the myofilaments to the matrix and the cardiac chambers, the cytoskeleton may also be important for propagating external physical signals into the cell.2Mutations in a growing list of cytoskeletal genes are associated with cardiomyopathies. Disruption of desmin, plakoglobin, N-cadherin, plectin, and vinculin all produce a dilated cardiac phenotype with impaired function, either in fetal development or after birth.3,4,5 These are elements of the cytoskeleton that connect intracellular structures with the extracellular matrix, and thus are likely force-transmitting components in the myocyte. Originally, Chien6 proposed that defects in the cytoskeletal component of the myocyte result in a dilated cardiomyopathic phenotype, whereas mutations in the sarcomeric proteins typically generate a pattern of hypertrophic cardiomyopathy with preserved ventricular systolic function in addition to the myocyte hypertrophy and disarray.7 But as more data have accumulated, the picture has become more complex, and cytoskeletal defects have been implicated in hypertrophic as well as dilated cardiomyopathies.8Cytoskeletal proteins have been implicated in several load-sensing pathways, and there is evidence that cytoskeletal proteins play a critical role in biomechanical signaling and may be involved with ventricular dilation and heart failure.9,10 These studies have led to the hypothesis that there may exist a common pathway to cardiac dilation and failure, and the critical components of this “failure transition”11 …" @default.
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• W2141195909 date "2006-01-06" @default.
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• W2141195909 title "Myocyte Shearing, Myocardial Sheets, and Microtubules" @default.
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• W2141195909 doi "https://doi.org/10.1161/01.res.0000200395.82480.8d" @default.
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