![]() ![]() In summary, FG-4592 treatment remarkably ameliorated hypertension and organ injury, possibly through stabilizing HIF1α and subsequently targeting eNOS, AGTR1, AGTR2, and oxidative stress. Moreover, FG-4592 treatment was hypotensive in L-NAME–induced hypertension. In vascular endothelial cells, FG-4592 upregulated total and phosphorylated eNOS. In vascular smooth muscle cells, FG-4592 treatment reduced angiotensin receptor type 1 (AGTR1) and increased AGTR2 levels, while preventing Ang II–induced oxidative stress. Additionally, the levels of thiobarbituric acid reactive substances (TBARs) in blood and urine were diminished by FG-4592 treatment. In an angiotensin II (Ang II) hypertension model, FG-4592 abolished hypertensive responses prevented vascular thickening, cardiac hypertrophy, and kidney injury downregulated AGTR1 expression and enhanced AGTR2, endothelial NO synthase (eNOS), and HIF1α protein levels in the aortas of mice. In the present study, we evaluate the effects of FG-4592 on hypertension. ![]() FG-4592 (Roxadustat) is a potentially novel, orally active small-molecule hypoxia-inducible factor (HIF) stabilizer and is being used clinically to treat chronic kidney disease (CKD) anemia. The prevalence of hypertension is increasing globally, while strategies for prevention and treatment of hypertension remain limited. ![]()
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