ArticleCell death & disease2024
N-acetylaspartate promotes glycolytic-to-oxidative fiber-type switch and resistance to atrophic stimuli in myotubes.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- A hydrogel ionic circuit electrical stimulation system to restore denervated muscle following long-gap peripheral nerve injury.Bioactive materials · 2027Article
- From neuronal marker to metabolic mediator: Expanding the functional landscape of N-acetylaspartate in the central nervous system and the periphery.Neural regeneration research · 2026Article
- Article
- Nutritional Strategies and Aging: Current Evidence and Future Directions.Molecules (Basel, Switzerland) · 2026Review
- Nutraceutical Potential of Astaxanthin in Muscle Metabolism, Exercise Adaptation, and Obesity.Nutrients · 2025Review
- Lipid Metabolism-Signaling Crosstalk in Metabolic Disease and Aging: Mechanisms and Therapeutic Targets.Nutrients · 2025Review
- Oxidative Stress in Neurodegenerative Disorders: A Key Driver in Impairing Skeletal Muscle Health.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
N-acetylaspartate (NAA) is a neuronal metabolite that can be extruded in extracellular fluids and whose blood concentration increases in several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS). Aspartoacylase (ASPA) is the enzyme responsible for NAA breakdown. It is abundantly expressed in skeletal muscle and most other human tissues, but the role of NAA catabolism in the periphery is largely neglected. Here we demonstrate that NAA treatment of differentiated C2C12 muscle cells increases lipid turnover, mitochondrial biogenesis and oxidative metabolism at the expense of glycolysis. These effects were ascribed to NAA catabolism, as CRISPR/Cas9 ASPA KO cells are insensitive to NAA administration. Moreover, the metabolic switch induced by NAA was associated with an augmented resistance to atrophic stimuli. Consistently with in vitro results, SOD1-G93A ALS mice show an increase in ASPA levels in those muscles undergoing the glycolytic to oxidative switch during the disease course. The impact of NAA on the metabolism and resistance capability of myotubes supports a role for this metabolite in the phenotypical adaptations of skeletal muscle in neuromuscular disorders.
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Registered trials
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