HIF-1, the Warburg Effect, and Macrophage/Microglia Polarization Potential Role in COVID-19 Pathogenesis.
HIF-1, the Warburg Effect, and Macrophage/Microglia Polarization Potential Role in COVID-19 Pathogenesis.
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DOI：
10.1155/2021/8841911
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发表时间：
2021
影响因子：
--
通讯作者：
Malara N
中科院分区：
文献类型：
--
作者：
Ferraro E;Germanò M;Mollace R;Mollace V;Malara N
尽管国际科学界致力于提高对2019冠状病毒病（COVID-19）的临床知识，但有关分子细节的知识仍然有限。本文综述了低氧在严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）适应不良免疫反应发病机制中的作用。感染的状态，严重的呼吸功能障碍，导致组织变得缺氧，由于细胞O2摄取和消耗之间的差异，类似于在许多实体癌的进展过程中在肿瘤组织内看到的。在这种情况下，COVID-19的异质性临床行为和多器官恶化被讨论为缺氧诱导因子-1（HIF-1）表达上调和与HIF-1相关的代谢重编程以及促炎性先天免疫反应激活的函数，与SARS-CoV-2病毒载量的增加无关。可能的药理学策略，旨在改善预后的O2。
Despite the international scientific community's commitment to improve clinical knowledge about coronavirus disease 2019 (COVID-19), knowledge regarding molecular details remains limited. In this review, we discuss hypoxia's potential role in the pathogenesis of the maladaptive immune reaction against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The state of infection, with serious respiratory dysfunction, causes tissues to become hypoxic due to a discrepancy between cellular O2 uptake and consumption similar to that seen within tumor tissue during the progression of numerous solid cancers. In this context, the heterogeneous clinical behavior and the multiorgan deterioration of COVID-19 are discussed as a function of the upregulated expression of the hypoxia-inducible factor-1 (HIF-1) and of the metabolic reprogramming associated with HIF-1 and with a proinflammatory innate immune response activation, independent of the increase in the viral load of SARS-CoV-2. Possible pharmacological strategies targeting O2 aimed to improve prognosis are suggested.
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