Elevated mechanical stress on cardiac muscle cells can trigger the activation of multiple signaling pathways involved in the disease progression of dilated cardiomyopathy (DCM) and chronic heart failure. The involvement of a potential defective mechanical stress sensor has been suggested, but the molecular components of the cardiac muscle stretch sensor have been unclear. In the December 27 Cell, Ralph Knöll and colleagues at the University of California at San Diego, La Jolla, USA, show that the cardiac mechanical stretch sensor machinery involves a cytoskeleton Z disc complex that is defective in a subset of human dilated cardiomyopathy (Cell, 111:943–955, December 27, 2002).

Knöll et al. performed a combination of biophysical and biochemical studies in muscle LIM protein (MLP) deficient cardiac muscle. They observed that MLP (a Z disc protein) interacted with telethonin (T-cap — a titin interacting protein), and had a selective role in mechanical stretch...

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