Perturbing this interaction with anti‐IGF2R increased IGF bioavailability to IGF1R and reduced the intracellular Ca 2+ concentration in dystrophic muscle cells, eventually resulting in an extremely significant amelioration of dystrophic muscle histology and vasculature defects and force performance.
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Blockade of IGF2R improves muscle regeneration and ameliorates Duchenne muscular dystrophy.
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