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Updated: Feb 26, 2026

Isolation and Differentiation of Primary Myoblasts from Mouse Skeletal Muscle Explants
Published on: October 15, 2019
Enhanced Energetic State and Protection from Oxidative Stress in Human Myoblasts Overexpressing BMI1
Silvia Dibenedetto1, Maria Niklison-Chirou1, Claudia P Cabrera2
1Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
Abstract:
The Polycomb group gene BMI1 is essential for efficient muscle regeneration in a mouse model of Duchenne muscular dystrophy, and its enhanced expression in adult skeletal muscle satellite cells ameliorates the muscle strength in this model. Here, we show that the impact of mild BMI1 overexpression observed in mouse models is translatable to human cells. In human myoblasts, BMI1 overexpression increases mitochondrial activity, leading to an enhanced energetic state with increased ATP production and concomitant protection against DNA damage both in vitro and upon xenografting in a severe dystrophic mouse model. These preclinical data in mouse models and human cells provide a strong rationale for the development of pharmacological approaches to target BMI1-mediated mitochondrial regulation and protection from DNA damage to sustain the regenerative potential of the skeletal muscle in conditions of chronic muscle wasting.
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