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Endogenous Oxidative Stress, but Not ER Stress, Induces Hypoxia-Independent VEGF(120) Release Through PI3K-Dependent Pathways in 3T3-L1 Adipocytes

机译:内源性氧化应激,而不是内质网应激,通过3T3-L1脂肪细胞中PI3K依赖性途径诱导缺氧依赖性VEGF(120)释放。

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摘要

Objective: Expressions of vascular endothelial growth factor (VEGF) are increased in obese adipocytes and is secreted from obese adipose tissue through hypoxia-independent pathways. Therefore, we investigated the hypoxia-independent mechanism underlying increased expression and release of VEGF in obese adipocytes.
机译:目的:肥胖脂肪细胞中血管内皮生长因子(VEGF)的表达增加,并通过与缺氧无关的途径从肥胖脂肪组织中分泌出来。因此,我们调查了肥胖脂肪细胞中VEGF表达增加和释放的低氧依赖性机制。

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