细胞通过激活三种不同激活时间的低氧诱导因子（HIFs）来对低氧作出反应。HIF过度表达会对细胞行为产生许多影响，如代谢改变、促进血管生成过程及诱导炎症反应。这些效应是癌细胞恶性进展的驱动力。在本研究中，我们详细研究了HIF1α和HIF2α的低氧诱导动态，这是最为研究的亚型之一，通过比较肿瘤细胞中的可用实验数据与得出的数学模型的结果进行了研究。然后，我们检查了当数学模型的无量纲参数组发生变化时，通过激活NFkB（核因子k-轻链激活增强剂B细胞）连接低氧和炎症的可能情景。通过这种方式，我们能够讨论为什么以及何时缺氧条件导致急性或慢性炎症状态。版权所有 © 2022 Elsevier Inc.。

Cells respond to hypoxia via the activation of three isoforms of Hypoxia Inducible Factors (HIFs), that are characterized by different activation times. HIF overexpression has many effects on cell behavior, such as change in metabolism, promotion of angiogenic processes and elicitation of a pro-inflammatory response. These effects are driving forces of malignant progression in cancer cells. In this work we study in detail hypoxia-induced dynamics of HIF1α and HIF2α, which are the most studied isoforms, comparing available experimental data on their evolution in tumor cells with the results obtained integrating the deduced mathematical model. Then, we examine the possible scenarios that characterize the link between hypoxia and inflammation via the activation of NFkB (Nuclear Factor k-light-chain-enhancer of activated B cells) when the dimensionless groups of parameters of the mathematical model change. In this way we are able to discuss why and when hypoxic conditions lead to acute or chronic inflammatory states.Copyright © 2022 Elsevier Inc. All rights reserved.