ArticleJournal of cachexia, sarcopenia and muscle2025
Fast Myosin Binding Protein-C Is a Vital Regulator in Young and Aged Fast Skeletal Muscle Homeostasis.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Muscle Diffraction at the Life Science X-ray Scattering Beamline.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundSkeletal muscle plays a vital role in voluntary movement and locomotion. Fast-twitch muscle fibres are characterized by their rapid contraction kinetics, high-force generation and a distinct gene expression profile compared to slow-twitch fibres. These fibres have a predominant expression of fast skeletal myosin binding protein-C (fMyBP-C). The role of fMyBP-C in skeletal muscle disease and aging remains poorly understood. To address this, our study employs mouse models with fMyBP-C ablation to investigate its significance in skeletal muscle physiology.
methodsSkeletal muscle samples from wild-type, db/db, MDX and ECC injury model (2-7 months) were analysed to determine the fMyBP-C levels. Next, male Mybpc2 knockout (C2
resultsThe expression of fMyBP-C was reduced (0.25-fold, p < 0.05) in the fast-twitch muscles of db/db mice, with a modest compensatory upregulation of slow skeletal MyBP-C (sMyBP-C) (~1.15-fold, p < 0.05). In MDX mice, fMyBP-C levels remain unchanged, whereas sMyBP-C levels were upregulated (~1.2-fold, p < 0.01). The fMyBP-C expression was 75% higher in the male skeletal muscles (p < 0.01) compared to females. Studies in young male C2
conclusionfMyBP-C is a critical regulator of muscle function and homeostasis in young male fast-twitch muscle fibres. Its absence exacerbates the impact of aging on muscle structure and function. These findings suggest that fMyBP-C could serve as a promising therapeutic target for mitigating muscle wasting associated with aging and disease.
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