Why the study?
Correct regulation of troponin and myosin contractile protein gene isoforms is critical for cardiac and skeletal muscle function, but the role of Prox1 in this regulation and its impact on muscle fiber type and cardiomyopathy was unclear.
Does Prox1 ablation cause dilated cardiomyopathy and slow-to-fast skeletal muscle fiber conversion in mice?
Population
Mouse models with cardiac-specific and skeletal muscle-specific Prox1 knockout
Comparison
Prox1 knockout vs control mice
Design
Preclinical conditional knockout study
Key result
Cardiac and skeletal muscle-specific knockout of Prox1 in mice caused marked overexpression of fast-twitch genes, leading to a slow- to fast-twitch muscle conversion and fatal dilated cardiomyopathy.
Authors
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Prox1 loss drives fatal DCM via fiber-type switch in mice; hypothesis-generating for its role in human cardiomyopathy, requiring translational studies.
Does Prox1 ablation cause dilated cardiomyopathy and slow-to-fast skeletal muscle fiber conversion in mice?
Prox1 is essential for repressing fast-twitch skeletal muscle genes in the heart and slow-twitch skeletal muscle, and its loss leads to fatal dilated cardiomyopathy.
Petchey et al. (2014) studied Dilated cardiomyopathy. Prox1 knockout vs. Wild-type (implied) was evaluated on Development of dilated cardiomyopathy and muscle fiber conversion. Cardiac and skeletal muscle-specific knockout of Prox1 in mice caused marked overexpression of fast-twitch genes, leading to a slow- to fast-twitch muscle conversion and fatal dilated cardiomyopathy.
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