Why the study?
Does mitochondrial division inhibitor (Mdivi) improve cardiac function and reduce fibrosis in wild type mice with pressure overload induced heart failure?
Population
Wild type mice with pressure overload induced heart failure created by ascending aortic banding
Comparison
Mitochondrial division inhibitor (Mdivi) vs Vehicle treated controls
Design
Preclinical
Follow-up
8 weeks
Authors
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Mdivi may improve function in murine pressure-overload HF; leaves open translation to human disease.
Does mitochondrial division inhibitor (Mdivi) improve cardiac function and reduce fibrosis in wild type mice with pressure overload induced heart failure?
Mdivi ameliorates pressure overload-induced heart failure in mice by inhibiting abnormal mitophagy, suggesting a potential novel therapeutic target.
Givvimani et al. (2012) studied this question.
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