Valsartan Attenuated Homocysteine-Induced Impaired Autophagy and ER Stress in Human Umbilical Vein Endothelial Cells

<div>A potential mechanism by which Hcy caused injury in HUVECs. Hcy-induced impaired autophagy and ER stress in HUVECs, which was associated with increased protein expression levels of AT1. AT1 block or silence improved autophagy and ER stress and attenuated apoptosis, at least partially, through suppressing GSK-3<i>β</i>/mTOR signaling pathway in HUVEC cells. Hcy: homocysteine; AT1: angiotensin II type 1 receptor; TDZD-8: 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione.</div>

Cardiovascular Therapeutics

fig8

Figure 8

Figure 8: Valsartan Attenuated Homocysteine-Induced Impaired Autophagy and ER Stress in Human Umbilical Vein Endothelial Cells 