Researchers reverse heart failure in Marfan mice

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Marfan hearts fail when exposed to stress levels well-tolerated by normal mice. Johns Hopkins Medicine researchers were able to reverse this heart failure with drug therapies

IN experiments with mice that have a rodent form of Marfan syndrome, Johns Hopkins researchers report that even modestly increasing stress on the animals’ hearts — at levels well-tolerated in normal mice — can initiate heart failure. The findings, described August 4 in the Journal of Clinical Inves­tigation Insight, revealed a novel cellular pathway in heart tissue that leads to heart failure and may serve as a model for a new stan­dard of treatment for children with this aggressive form of Marfan syndrome.

Marfan syndrome is a genetic disorder that affects connective tissue throughout the body, elon­gating limbs, fingers and toes, for example. However, its worst effects are in the heart’s blood vessels and valves. Aortic enlargement, heart valve leaks and heart failure — marked by heart enlargement and weakened pumping action – are all potentially life-threatening.

The Hopkins team’s interest in the mouse model grew out of the clinical experience of children with Marfan seen at The Johns Hopkins Hospital over decades.

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