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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 µg 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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Cox4i2 triggers an increase in reactive oxygen species, leading to ferroptosis and apoptosis in HHV7 infected Schwann cells