Abnormal trafficking of connexin 43: A key element in the development of LMNA cardiomyopathy


Compared with other forms of dilated cardiomyopathy, mutations in LMNA encoding nuclear A-type lamins are responsible for a more aggressive clinical course due to a high rate of malignant conduction defects. A better understanding of factors and mechanisms that drive conduction defects are crucial for generation of potential therapies. Inter-cellular communication is essential for proper cardiac function. Mechanical and electrical activities must synchronize so that the work of individual cardiomyocytes transforms into the pumping function of the heart.


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