期刊
CELL METABOLISM
卷 32, 期 3, 页码 437-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2020.07.007
关键词
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资金
- Sao Paulo Research Foundation -FAPESP [2015/15626-8, 2016/23328-0, 2016/18031-8, 2018/22505-0, 20/04579-7, 2020/04746-0, 2019/06372-3, 2020/04558-0, 2020/04919-2, 2020/04583-4, 2017/01184-9, 2020/04522-5, 2019/00098-7]
- Fundo de Apoio ao Ensino, Pesquisa e Extensao (FAEPEX), Unicamp [2274/20]
- Brazilian National Council for Scientific and Technological Development - CNPq
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - Brazil (CAPES) [001]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [20/04579-7] Funding Source: FAPESP
COVID-19 can result in severe lung injury. It remained to be determined why diabetic individuals with uncontrolled glucose levels are more prone to develop the severe form of COVID-19. The molecular mechanism underlying SARS-CoV-2 infection and what determines the onset of the cytokine storm found in severe COVID-19 patients are unknown. Monocytes and macrophages are the most enriched immune cell types in the lungs of COVID-19 patients and appear to have a central role in the pathogenicity of the disease. These cells adapt their metabolism upon infection and become highly glycolytic, which facilitates SARS-CoV-2 replication. The infection triggers mitochondrial ROS production, which induces stabilization of hypoxia-inducible factor-1 alpha (HIF-1 alpha) and consequently promotes glycolysis. HIF-1 alpha-induced changes in monocyte metabolism by SARSCoV-2 infection directly inhibit T cell response and reduce epithelial cell survival. Targeting HIF-1 alpha may have great therapeutic potential for the development of novel drugs to treat COVID-19.
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