In cardiomyopathy, the heart becomes progressively enlarged and weak, and often arrhythmogenic, which can lead to heart failure. This common condition remains difficult to treat. The genetic contributors to cardiomyopathy are not fully recognized, although cell-cell junctions, which allow for cardiocyte communication and coordinate function, are often disrupted in the disease. Seeger et al. recently identified the protein myozap (myocardium-enriched zonula occludens-1-associated protein), which is highly expressed in the myocardium and localizes to intercalated discs at cell-cell junctions. Myozap links signaling at the intercalated disc to cardiac gene regulation by binding to a negative regulator of RhoA phosphatase, which modulates both intracellular cytoskeletal dynamics and nuclear gene transcription. Genetic knockdown of the myozap ortholog in zebrafish disrupts cardiac contractility and induces cardiomyopathy, suggesting a potential role for myozap in human heart disease.
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RESEARCH HIGHLIGHT| 08 March 2010
Cardiomyopathy: myozap for the heart
Online Issn: 1754-8411
Print Issn: 1754-8403
Dis Model Mech (2010) 3 (3-4): 122.
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Cardiomyopathy: myozap for the heart. Dis Model Mech 8 March 2010; 3 (3-4): 122. doi:
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