COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine stormopen access
- Authors
- Lee, Wonhwa; Ahn, June Hong; Park, Hee Ho; Kim, Hong Nam; Kim, Hyelim; Yoo, Youngbum; Shin, Hyosoo; Hong, Kyung Soo; Jang, Jong Geol; Park, Chun Gwon; Choi, Eun Young; Bae, Jong-Sup; Seo, Young-Kyo
- Issue Date
- Sep-2020
- Publisher
- SPRINGERNATURE
- Citation
- SIGNAL TRANSDUCTION AND TARGETED THERAPY, v.5, no.1, pp.1 - 11
- Indexed
- SCIE
SCOPUS
- Journal Title
- SIGNAL TRANSDUCTION AND TARGETED THERAPY
- Volume
- 5
- Number
- 1
- Start Page
- 1
- End Page
- 11
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/187332
- DOI
- 10.1038/s41392-020-00292-7
- ISSN
- 2095-9907
- Abstract
- Sterol regulatory element binding protein-2 (SREBP-2) is activated by cytokines or pathogen, such as virus or bacteria, but its association with diminished cholesterol levels in COVID-19 patients is unknown. Here, we evaluated SREBP-2 activation in peripheral blood mononuclear cells of COVID-19 patients and verified the function of SREBP-2 in COVID-19. Intriguingly, we report the first observation of SREBP-2 C-terminal fragment in COVID-19 patients' blood and propose SREBP-2 C-terminal fragment as an indicator for determining severity. We confirmed that SREBP-2-induced cholesterol biosynthesis was suppressed by Sestrin-1 and PCSK9 expression, while the SREBP-2-induced inflammatory responses was upregulated in COVID-19 ICU patients. Using an infectious disease mouse model, inhibitors of SREBP-2 and NF-kappa B suppressed cytokine storms caused by viral infection and prevented pulmonary damages. These results collectively suggest that SREBP-2 can serve as an indicator for severity diagnosis and therapeutic target for preventing cytokine storm and lung damage in severe COVID-19 patients.
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