ArticleiScience2024
MEK-inhibitors decrease Nfix in muscular dystrophy but induce unexpected calcifications, partially rescued with Cyanidin diet.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 2 citations in OpenAlex.
- Dynamic NFIX Promoter Usage Shapes Stem and Committed Myogenic States.International journal of molecular sciences · 2026Article
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Crocetin Attenuates Fibroblast-to-Myofibroblast Transition after Myocardial Infarction in Mice by Regulating Autophagy.Cardiovascular drugs and therapy · 2026Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscular dystrophies (MDs) are incurable genetic myopathies characterized by progressive degeneration of skeletal muscles. Dystrophic mice lacking the transcription factor Nfix display morphological and functional improvements of the disease. Recently, we demonstrated that MAPK signaling pathway positively regulates Nfix in muscle development and that Cyanidin, a natural antioxidant molecule, strongly ameliorates the pathology. To explore a synergistic approach aimed at treating MDs, we administered Trametinib, a clinically approved MEK inhibitor, alone or combined with Cyanidin to adult
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Registered trials
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