Role of Family with Sequence Similarity 3A in High Glucose-induced Oxidative Damage of Human Umbilical Vein Endothelial Cells.

/(μg protein·min)] of siFam3A control group (t=19.876,P=0.003), which was significantly lower than that of siNT high glucose group (t=21.444,P=0.002). The relative expression of P-p38 in siNT high glucose group, siFam3A control group, and siFam3A high glucose group was 2.239±0.353, 0.816±0.120, and 1.160±0.185, respectively; thus, it was significantly higher in the siNT high glucose group than in siNT control group (t=6.075,P=0.026); in addition, it was significantly higher in the siFam3A high glucose group than in siFam3A control group (t=6.242,P=0.024) and significantly lower than in siNT high glucose group (t=9.686,P=0.010). Conclusions High glucose can induce high expression of Fam3A in HUVECs. Knockdown of Fam3A gene expression can exacerbate the decrease of ATP synthesis and mitochondrial OCR caused by high glucose and promote the generation of ROS in high glucose. Fam3A may regulate high glucose-induced ROS production in HUVECs via the p38 MAPK signaling pathway.