Centre for Cellular and Molecular Physiology, Nuffield Department of Medicine, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, United Kingdom.
Chemistry Research Laboratory, Department of Chemistry, University of Oxford, 12 Mansfield Road, Oxford OX1 3TA, United Kingdom.
Mol Aspects Med. 2016 Feb-Mar;47-48:54-75. doi: 10.1016/j.mam.2016.01.001. Epub 2016 Jan 11.
In human cells oxygen levels are 'sensed' by a set of ferrous iron and 2-oxoglutarate dependent dioxygenases. These enzymes regulate a broad range of cellular and systemic responses to hypoxia by catalysing the post-translational hydroxylation of specific residues in the alpha subunits of hypoxia inducible factor (HIF) transcriptional complexes. The HIF hydroxylases are now the subject of pharmaceutical targeting by small molecule inhibitors that aim to activate or augment the endogenous HIF transcriptional response for the treatment of anaemia and other hypoxic human diseases. Here we consider the rationale for this therapeutic strategy from the biochemical, biological and medical perspectives. We outline structural and mechanistic considerations that are relevant to the design of HIF hydroxylase inhibitors, including likely determinants of specificity, and review published reports on their activity in pre-clinical models and clinical trials.
在人类细胞中,一组亚铁离子和 2-氧代戊二酸依赖性双氧酶“感知”氧气水平。这些酶通过催化缺氧诱导因子 (HIF) 转录复合物的α亚基中特定残基的翻译后羟化作用,调节细胞和全身对缺氧的广泛反应。HIF 羟化酶现在是小分子抑制剂靶向治疗的对象,这些抑制剂旨在激活或增强内源性 HIF 转录反应,以治疗贫血和其他人类缺氧疾病。在这里,我们从生化、生物学和医学的角度考虑这种治疗策略的基本原理。我们概述了与 HIF 羟化酶抑制剂设计相关的结构和机制考虑因素,包括可能决定特异性的因素,并回顾了它们在临床前模型和临床试验中的活性的已发表报告。