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Thus, although EE/ICA-induced myotube hypertrophy via the modulation of IGF-1R phosphorylation has been confirmed in this study, a direct IGF-1R interation or mediated through other underlying mechanisms require further clarification
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Studies have shown that UPR is an underlying cellular mechanism of various human diseases such as ischemia, Friedreich’s ataxia, Alzheimer’s disease, type 2 diabetes, and cystic fibrosis [131,132,133]
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