Key result
Expression of a caspase-resistant desmin mutant (D263E) attenuated cardiomyocyte apoptosis, prevented left ventricular wall thinning, and improved heart function in a mouse model of cardiomyopathy.
Why the study?
Does expression of a caspase-resistant desmin mutant prevent aggregate formation and improve cardiac function in a mouse model of TNF-alpha-induced cardiomyopathy?
Does expression of a caspase-resistant desmin mutant prevent aggregate formation and improve cardiac function in a mouse model of TNF-alpha-induced cardiomyopathy?
Preventing caspase-6 cleavage of desmin attenuates aggregate formation and improves cardiac function in a mouse model of TNF-alpha-induced cardiomyopathy.
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May support desmin stabilization in experimental cardiomyopathy; leaves open translation to human disease.
Panagopoulou et al. (2008) studied TNF-alpha-induced cardiomyopathy. Cardiac-restricted expression of a desmin mutant (D263E) was evaluated on Cardiomyocyte apoptosis, left ventricular wall thinning, and heart function. Expression of a caspase-resistant desmin mutant (D263E) attenuated cardiomyocyte apoptosis, prevented left ventricular wall thinning, and improved heart function in a mouse model of cardiomyopathy.
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