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Firstly, treatment of BMECs with MGO leads to an activation of stress-associated pathways, characterized by an increase in phosphorylation of extracellular signal-regulated kinase (ERK) [59], c-Jun N-terminal kinase (JNK) [59, 64], and p38 [59], which are known responders to stress stimuli and affect endothelial cells by altering, for instance, barrier function, protein synthesis, and apoptosis [73]

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