ArticleFrontiers in cell and developmental biology2025
Zinc transporter ZIP10 supports zinc homeostasis and myoglobin biosynthesis in differentiating C2C12 myoblasts.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Zinc is an essential micronutrient required for diverse cellular processes, including skeletal muscle development and regeneration. Although skeletal muscle contains a large proportion of total body zinc, the mechanisms that maintain zinc homeostasis during myoblast differentiation, particularly under zinc-limited conditions, remain poorly understood. Methods: We investigated ZIP10 (SLC39A10) as the primary zinc importer responsible for maintaining intracellular zinc homeostasis under fluctuating zinc conditions during C2C12 myoblast differentiation. Zinc levels were modulated using zinc chelation or supplementation, and ZIP10 expression was repressed by gene silencing. Molecular and functional signatures of myogenesis were assessed through gene and protein expression analyses and nitric oxide (NO) metabolite profiling. Result: Zinc deficiency markedly reduced the expression of the muscle-specific transcription factor Conclusion: These findings identify ZIP10 as an important zinc importer that supports intracellular zinc supply and
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