2018
DOI: 10.1016/j.cmet.2018.06.011
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Mitofusin 2 Regulates Axonal Transport of Calpastatin to Prevent Neuromuscular Synaptic Elimination in Skeletal Muscles

Abstract: Skeletal muscles undergo atrophy in response to diseases and aging. Here we report that mitofusin 2 (Mfn2) acts as a dominant suppressor of neuromuscular synaptic loss to preserve skeletal muscles. Mfn2 is reduced in spinal cords of transgenic SOD1 and aged mice. Through preserving neuromuscular synapses, increasing neuronal Mfn2 prevents skeletal muscle wasting in both SOD1 and aged mice, whereas deletion of neuronal Mfn2 produces neuromuscular synaptic dysfunction and skeletal muscle atrophy. Neuromuscular s… Show more

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Cited by 42 publications
(46 citation statements)
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“…Calpastatin, an endogenous inhibitor of calcium-dependent cysteine protease calpain, is involved in protein degradation, neuromuscular function regulation [38], and axon survival [58]. A noteworthy increase of the calpastatin level was observed in obestatin-treated sciatic nerves 12d post-injury ( Fig.…”
Section: Resultsmentioning
confidence: 94%
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“…Calpastatin, an endogenous inhibitor of calcium-dependent cysteine protease calpain, is involved in protein degradation, neuromuscular function regulation [38], and axon survival [58]. A noteworthy increase of the calpastatin level was observed in obestatin-treated sciatic nerves 12d post-injury ( Fig.…”
Section: Resultsmentioning
confidence: 94%
“…The role of Mfn2 and mitochondria in the axonal transport of calpastatin is su cient to inhibit localized calpain activation, axon degradation, neuromuscular synaptic loss and muscle atrophy upon nerve injury [38]. Remarkably, the ratio of acetylcholine receptor (AChR)-rich postsynaptic sites on myo bers was increased in TA muscles after sciatic nerve injury under obestatin administration (Fig.…”
Section: Resultsmentioning
confidence: 98%
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