缺氧诱导因子
红细胞生成
缺氧(环境)
血管生成
转录因子
下调和上调
生物
新陈代谢
癌症研究
细胞生物学
生物化学
内科学
化学
医学
贫血
基因
氧气
有机化学
作者
Peppi Koivunen,Thomas Kietzmann
标识
DOI:10.1016/j.molmed.2018.10.004
摘要
Hypoxia-inducible factor prolyl 4-hydroxylases (HIF-P4Hs, also known as PHDs or EglNs) are enzymes that act as cellular oxygen sensors. Inhibition of HIF-P4Hs leads to stabilization of hypoxia-inducible transcription factors (HIFs), which initiates a gene expression program that allows organisms to cope with low oxygen levels and restore tissue oxygenation. This involves, for example, upregulation of erythropoiesis and angiogenesis, modulation of inflammatory responses, and reprogramming of metabolism. Currently, several pharmacological HIF-P4H inhibitors are in clinical trials mainly for renal anemia. However, recent data suggest that HIF-P4H inhibitors could also be considered to treat metabolic disorders. Here, we discuss the potential of targeting HIF-P4Hs and the HIF pathway for the treatment of obesity, metabolic syndrome, atherosclerosis, and fatty liver diseases (FLDs).
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