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Moreover, when mice were pre-treated with vehicle or L2-Cmu (20 mg/kg) by intraperitoneal (i.p.) injection, and then challenged with an intravenous (i.v.) bolus of saline or 5 g IGF-1, L2-Cmu was able to modulate IGF-1R activation in vivo, as demonstrated by a near complete inhibition of IGF-1R phosphorylation in lung and ~70% inhibition in heart (Fig

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Its future development will depend heavily on advances in cell engineering, particularly in delivery systems, mitochondrial engineering, and targeting strategies, while also requiring continued progress in materials science to improve stabilization, controlled release, and in vivo protection of transplanted mitochondria