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Abstract
The fruit fly, Drosophila melanogaster, is an excellent model system that has a vast
set of molecular tools and mutants to dissect the genetic pathways that are responsible
for the normal and abnormal cardiac function. While the majority of studies have focused
on heart development in the Drosophila embryo, attention has recently focused on the
structure and function of the adult fly heart as a model of human heart failure. Here
we review strategies to identify novel genes and pathways that cause or modify dilated
cardiomyopathy in adult Drosophila.