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ApoC3 was also reported to exert pro-inflammatory effects on components of the vascular wall, but via distinct mechanisms (Table 1)
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When -MSH binds to MC1R, it triggers the production of intracellular cAMP, which activates protein kinases C and A, leading to the activation of the MAPK and JAK-STAT pathways
TJ loss increased cell motility, and subsequent AJ loss further up-regulated that
