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Schema of mechanism of DMY attenuates TNF-α-induced endothelial dysfunction. In response to TNF-α, miR-21 expression is increased and inhibits DDAH1, an effect that increases downstream ADMA concentration, which resulted in decreasing phosphorylation of eNOS and NO production and led to endothelial dysfunction. In contrast, DMY represses TNF-α-induced miR-21 expression and restores endothelial function.
