https://www.selleckchem.com/pr....oducts/ertugliflozin
Overexpressed miR-328-3p obviously alleviated ox-LDL induced inhibition on cell viability, migration and invasion, stimulation on apoptosis, autophagy as well as inflammation in HUVECs. FOXO4 was elevated in ox-LDL HUVECs, and functional assay indicated that FOXO4 aggravated ox-LDL induced HUVECs impairment. In addition, FOXO4 was a target of miR-328-3p in HUVECs; rescue experiments suggested miR-328-3p could protect HUVECs against ox-LDL induced injury via regulating FOXO4. CONCLUSIONS MiR-328-3p protected vascular endothelial ce
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