ArticleInternational journal of molecular sciences2025
SMURF1-Induced Ubiquitination of FTH1 Disrupts Iron Homeostasis and Suppresses Myogenesis.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Ferroptosis in skeletal muscle: from molecular mechanisms to therapeutic interventions.Journal of orthopaedic translation · 2026Review
- MDM2 Alters Cellular Iron Homeostasis by Promoting the Degradation of Proteins Involved in Iron Storage and Iron Export.Current issues in molecular biology · 2026Article
- Ferroptosis in musculoskeletal disorders: Emerging mechanisms and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Age-related transcriptional drift and physiological adaptation in long-living Ames dwarf skeletal muscle.NAR molecular medicine · 2026Article
- The D826V point mutation inFrontiers in cell and developmental biology · 2026Article
- Current Progress in the Role of Ferroptosis in Skeletal Muscle Atrophy.Mediators of inflammation · 2026Review
- Lactylation-mediated miRNA regulation in cancer therapy resistance.Journal of translational medicine · 2025Review
- Ferroptosis-related oxidative stress activation in the acute phase of Kawasaki disease.Frontiers in immunology · 2025Article
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14 authors.
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Abstract
Ferritin heavy chain 1 (FTH1) is pivotal in the storage, release, and utilization of iron, plays a crucial role in the ferroptosis pathway, and exerts significant impacts on various diseases. Iron influences skeletal muscle development and health by promoting cell growth, ensuring energy metabolism and ATP synthesis, maintaining oxygen supply, and facilitating protein synthesis. However, the precise molecular mechanisms underlying iron's regulation of skeletal muscle growth and development remain elusive. In this study, we demonstrated that the conditional knockout (cKO) of FTH1 in skeletal muscle results in muscle atrophy and impaired exercise endurance. In vitro studies using FTH1 cKO myoblasts revealed notable decreases in GSH concentrations, elevated levels of lipid peroxidation, and the substantial accumulation of Fe
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