Cell responses to reduced oxygen supply (hypoxia) are largely mediated by hypoxia-inducible transcription factors (HIFs). The pathophysiological role of the HIF pathway is driven by its ability to potentiate key biological processes as part of the adaptation to hypoxia, such as erythropoiesis and angiogenesis. Moreover, the role of HIF signaling in the reprogramming of cell metabolism is also critical to understand the role of these transcription factors in health and disease. In this regard, HIFs reprogram oxidative metabolism of glucose and fatty acids, offering a molecular mechanism by which the HIF pathway can help cells become more tolerant of redox stress during hypoxic/ischemic episodes. However, the way in which HIFs influence amino acid metabolism and its pathophysiology consequences have been less well explored. Here we review recent studies about the role of the HIF1α and HIF2α isoforms in amino acid metabolism, which provides insight to better understand how these factors can influence cell autonomous proliferation and cellular tolerance to hypoxia.

细胞对氧气供应减少（缺氧）的反应在很大程度上由缺氧诱导的转录因子（HIF）介导。HIF途径的病理生理作用是由其增强关键生物学过程的能力所驱动的，这是适应低氧（如红细胞生成和血管生成）的一部分。此外，HIF信号在细胞代谢重编程中的作用对于理解这些转录因子在健康和疾病中的作用也至关重要。在这方面，HIF重新编程葡萄糖和脂肪酸的氧化代谢，从而提供一种分子机制，通过该机制，HIF途径可以帮助细胞在缺氧/缺血性发作期间变得更加耐受氧化还原应激。但是，HIF影响氨基酸代谢及其病理生理后果的方式尚未得到很好的研究。