氧化应激
血管生成
缺氧诱导因子
炎症
肾脏疾病
PEDF公司
视网膜色素上皮
细胞因子
血管内皮生长因子
视网膜
缺氧(环境)
生物
癌症研究
医学
内分泌学
免疫学
内科学
化学
基因
生物化学
有机化学
氧气
血管内皮生长因子受体
作者
Tamás Gáll,Dávid Pethő,Annamária Nagy,Szilárd Póliska,György Balla,József Balla
出处
期刊:Cells
[Multidisciplinary Digital Publishing Institute]
日期:2025-07-21
卷期号:14 (14): 1121-1121
标识
DOI:10.3390/cells14141121
摘要
Chronic kidney disease (CKD)-associated anemia is a global health concern and is linked to vascular and ocular complications. Hypoxia-inducible factor (HIF) stabilizers, or HIF prolyl hydroxylase inhibitors (PHIs), are promising candidates for the treatment of CKD-associated anemia. Since hypoxia and angiogenesis are involved in eye diseases, this study examined the effects of HIF-PHIs on metabolism and gene expression in retinal pigment epithelium (RPE) cells. Results revealed that PHIs differentially induced angiogenic (VEGFA, ANG) and glycolytic (PDK1, GLUT1) gene expression, with Roxadustat causing the strongest transcriptional changes. However, Roxadustat-induced angiogenic signals did not promote endothelial tube formation. Moreover, it did not induce oxidative stress, inflammation, or significant antioxidant gene responses in ARPE-19 cells. Roxadustat also reduced the inflammatory cytokine response to tumor necrosis factor-α, including IL-6, IL-8, and MCP-1, and did not exacerbate VEGF expression under high-glucose conditions. Overall, Roxadustat triggered complex gene expression changes without promoting inflammation or oxidative stress in RPE cells. Despite these findings, ophthalmologic monitoring is advised during PHI treatment in CKD patients receiving HIF-PHIs.
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