ArticleAntioxidants (Basel, Switzerland)2021
The Atrophic Effect of 1,25(OH)
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Antioxidant Interventions on Muscle Function and Mass in Aging-Related Muscle Decline: A Systematic Review of Preclinical and Clinical Evidence.Antioxidants (Basel, Switzerland) · 2026Review
- Vitamin D binding protein induces skeletal muscle atrophy and contributes to cancer-associated muscle wasting independently of vitamin D status in preclinical models.Nature communications · 2026Article
- TSC-associated microglial hyperactivity: enhanced calcium signaling, metabolism, and phagocytosis.Acta neuropathologica · 2026Article
- Diet-Derived Advanced Glycation End-Products (AGEs) Induce Muscle Wasting In Vitro, and a StandardizedAntioxidants (Basel, Switzerland) · 2025Article
- Astroglial calcium signaling and homeostasis in tuberous sclerosis complex.Acta neuropathologica · 2024Article
- Valine improves mitochondrial function and protects against oxidative stress.Bioscience, biotechnology, and biochemistry · 2024Article
- Bioconversion of vitamin DAMB Express · 2023Article
- Mechanism of skeletal muscle atrophy after spinal cord injury: A narrative review.Frontiers in nutrition · 2023Review
- Potential Therapeutic Strategies for Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022Review
- PGC-1α overexpression is not sufficient to mitigate cancer cachexia in either male or female mice.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Dysfunctional mitochondrial metabolism has been linked to skeletal muscle loss in several physio-pathological states. Although it has been reported that vitamin D (VD) supports cellular redox homeostasis by maintaining normal mitochondrial functions, and VD deficiency often occurs in conditions associated with skeletal muscle loss, the efficacy of VD supplementation to overcome muscle wasting is debated. Investigations on the direct effects of VD metabolites on skeletal muscle using C2C12 myotubes have revealed an unexpected pro-atrophic activity of calcitriol (1,25VD), while its upstream metabolites cholecalciferol (VD3) and calcidiol (25VD) have anti-atrophic effects. Here, we investigated if the atrophic effects of 1,25VD on myotubes depend on its activity on mitochondrial metabolism. The impact of 1,25VD and its upstream metabolites VD3 and 25VD on mitochondria dynamics and the activity of C2C12 myotubes was evaluated by measuring mitochondrial content, architecture, metabolism, and reactive oxygen species (ROS) production. We found that 1,25VD induces atrophy through protein kinase C (PKC)-mediated ROS production, mainly of extramitochondrial origin. Consistent with this, cotreatment with the antioxidant N-acetylcysteine (NAC), but not with the mitochondria-specific antioxidant mitoTEMPO, was sufficient to blunt the atrophic activity of 1,25VD. In contrast, VD3 and 25VD have antioxidant properties, suggesting that the efficacy of VD supplementation might result from the balance between atrophic pro-oxidant (1,25VD) and protective antioxidant (VD3 and 25VD) metabolites.
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Registered trials
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