Journal
HUMAN MOLECULAR GENETICS
Volume 18, Issue 2, Pages 318-327Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddn358
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Funding
- NIH [T32 GM65823, HL81587, AR48179-01]
- Edith Hyde Fellowship
- Ursula Mandel Fellowship
- Harold and Lillian Kraus American Heart Pre-doctoral Fellowship
- Training in Cardiovascular Physiology and Pharmacology Training [5T32HL007444-27]
- American Heart Association
- Muscular Dystrophy Association [MDA3704]
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Duchenne muscular dystrophy is caused by dystrophin mutations that lead to structural instability of the sarcolemma membrane, myofiber degeneration/regeneration and progressive muscle wasting. Here we show that myogenic Akt signaling in mouse models of dystrophy promotes increased expression of utrophin, which replaces the function of dystrophin thereby preventing sarcolemma damage and muscle wasting. In contrast to previous suggestions that increased Akt in dystrophy was a secondary consequence of pathology, our findings demonstrate a pivotal role for this signaling pathway such that modulation of Akt can significantly affect disease outcome by amplification of existing, physiological compensatory mechanisms.
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