Medicine and Health

N-acetylaspartate promotes glycolytic-to-oxidative fiber-type switch and resistance to atrophic stimuli in myotubes

S. Castelli, E. Desideri, et al.

N-acetylaspartate (NAA) treatment in C2C12 myotubes significantly enhances lipid turnover, mitochondrial biogenesis, and oxidative metabolism, while improving resistance to atrophic stimuli. This groundbreaking research conducted by Serena Castelli, Enrico Desideri, and colleagues unveils the critical role of NAA in transforming muscle response in neurodegenerative diseases like amyotrophic lateral sclerosis (ALS).

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Abstract

N-acetylaspartate (NAA), a neuronal metabolite, increases in blood during neurodegenerative diseases like amyotrophic lateral sclerosis (ALS). This study shows that NAA treatment in C2C12 myotubes increases lipid turnover, mitochondrial biogenesis, and oxidative metabolism, reducing glycolysis. This effect depends on NAA catabolism via aspartoacylase (ASPA), as CRISPR/Cas9 ASPA knockout cells are unresponsive. NAA treatment also increases resistance to atrophic stimuli. ALS mice show increased ASPA in muscles undergoing a glycolytic-to-oxidative switch, supporting NAA's role in skeletal muscle adaptation in neuromuscular disorders.

Publisher

Cell Death and Disease

Published On

Sep 19, 2024

Authors

Serena Castelli, Enrico Desideri, Leonardo Laureti, Federica Felice, Angela De Cristofaro, Silvia Scaricamazza, Giacomo Lazzarino, Maria Rosa Ciriolo, Fabio Ciccarone

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