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. 2018 Jul 16;9:473. doi: 10.3389/fneur.2018.00473

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Copyright © 2018 Chakraborty, Llamusi and Artero.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The physiopathological parallelisms between model fly heart and diseased human heart. Repeat expansion in both fly and patient heart causes a marked reduction in the lifespan. The expression of the repeats in the fly heart causes conduction defects, arrhythmia and contractility defects as observed in DM patients. At the molecular level, microsatellite expansion in the heart causes Muscleblind sequestration in the ribonuclear foci and this sequestration leads to misregulation in alternative splicing both in fly and human heart. Induction in the autophagy is also observed in the fly heart.