ArticleEMBO molecular medicine2021
MOTS-c promotes phosphorodiamidate morpholino oligomer uptake and efficacy in dystrophic mice.
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- MOTS-c modulates pancreatic islet function in rats and pigs in vitro.Histochemistry and cell biology · 2025Article
- MOTS-c Serum Concentration Positively Correlates with Lower-Body Muscle Strength and Is Not Related to Maximal Oxygen Uptake-A Preliminary Study.International journal of molecular sciences · 2023Article
- Duchenne muscular dystrophy: pathogenesis and promising therapies.Journal of neurology · 2023Review
- Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.Journal of translational medicine · 2023Review
- MOTS-c Functionally Prevents Metabolic Disorders.Metabolites · 2023Review
- The Mitochondrial-Derived Peptide MOTS-c Attenuates Oxidative Stress Injury and the Inflammatory Response of H9c2 Cells Through the Nrf2/ARE and NF-κB Pathways.Cardiovascular engineering and technology · 2022Article
- Cardio-respiratory and phenotypic rescue of dystrophin/utrophin-deficient mice by combination therapy.EMBO reports · 2022Article
- MOTS-c promotes phosphorodiamidate morpholino oligomer uptake and efficacy in dystrophic mice.EMBO molecular medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antisense oligonucleotide (AO)-mediated exon-skipping therapies show promise in Duchenne muscular dystrophy (DMD), a devastating muscular disease caused by frame-disrupting mutations in the DMD gene. However, insufficient systemic delivery remains a hurdle to clinical deployment. Here, we demonstrate that MOTS-c, a mitochondria-derived bioactive peptide, with an intrinsic muscle-targeting property, augmented glycolytic flux and energy production capacity of dystrophic muscles in vitro and in vivo, resulting in enhanced phosphorodiamidate morpholino oligomer (PMO) uptake and activity in mdx mice. Long-term repeated administration of MOTS-c (500 μg) and PMO at the dose of 12.5 mg/kg/week for 3 weeks followed by 12.5 mg/kg/month for 3 months (PMO-M) induced therapeutic levels of dystrophin expression in peripheral muscles, with up to 25-fold increase in diaphragm of mdx mice over PMO alone. PMO-M improved muscle function and pathologies in mdx mice without detectable toxicity. Our results demonstrate that MOTS-c enables enhanced PMO uptake and activity in dystrophic muscles by providing energy and may have therapeutic implications for exon-skipping therapeutics in DMD and other energy-deficient disorders.
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