Key result
Human dilated cardiomyopathy is characterized by increased variability in cardiomyocyte size and re-expression of the embryonic EH-myomesin isoform, which likely contributes to decreased functional output.
Provides a structural mechanism for reduced contractile function in dilated cardiomyopathy; leaves open whether targeting embryonic.
Hypertrophic cardiomyopathy is characterised by a histological phenotype of myocyte disarray, but heart tissue samples from patients with dilated cardiomyopathy (DCM) often look comparatively similar to those from healthy individuals apart from conspicuous regions of fibrosis and necrosis. We have previously investigated subcellular alterations in the cytoarchitecture of mouse models of dilated cardiomyopathy and found that both the organisation and composition of the intercalated disc, i.e. the specialised type of cell-cell contact in the heart, is altered. There is also is a change in the composition of the M-band of the sarcomere due to an expression shift towards the more extensible embryonic heart (EH)-myomesin isoform. Analysis of human samples from the Sydney Human Heart Tissue Bank have revealed similar structural findings and also provided evidence for a dramatic change in overall cardiomyocyte size control, which has also been seen in the mouse. Together these changes in cytoarchitecture probably contribute to the decreased functional output that is seen in DCM.
No takes yet. Share an insight, caveat, or question.
Pluess et al. (2014) conducted a review in Dilated cardiomyopathy (n=54). Human dilated cardiomyopathy is characterized by increased variability in cardiomyocyte size and re-expression of the embryonic EH-myomesin isoform, which likely contributes to decreased functional output.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: