1. Contribution of STAT3 to the pathogenesis of COVID-19.
- Author
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Jafarzadeh, Abdollah, Nemati, Maryam, and Jafarzadeh, Sara
- Subjects
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COVID-19 , *COVID-19 treatment , *COVID-19 pandemic , *LYMPHOPENIA , *CYTOKINE release syndrome , *PULMONARY fibrosis - Abstract
Hyper-inflammatory responses, lymphopenia, unbalanced immune responses, cytokine storm, large viral replication and massive cell death play fundamental roles in the pathogenesis of COVID-19. Extreme production of many kinds of pro-inflammatory cytokines and chemokines occur in severe COVID-19 that called cytokine storm. Signal transducer and activator of transcription-3 (STAT-3) present in the cytoplasm in an inactive form and can be stimulated by a vast range of cytokines, chemokines and growth factors. Thus, STAT-3 can participate in the induction of inflammatory responses during coronavirus infections. STAT-3 can also suppress anti-virus interferon response and induce unbalanced anti-virus adaptive immune response, through influencing Th17-, Th1-, Treg-, and B cell-mediated functions. Furthermore, STAT-3 can contribute to the M2 macrophage polarization, lung fibrosis and thrombosis. Moreover, STAT-3 may be directly targeted by some virus-derived protein and operate as a pro-viral or anti-viral element in a virus-specific process. Here, the possible contribution of STAT-3 to the pathogenesis of COVID-19 was explained, while providing potential approaches to target this transcription factor in an attempt for COVID-19 treatment. • STAT-3 can be activated by numerous cytokines during COVID-19. • STAT-3 is hyper-activated and can play a central role in COVID-19 pathogenesis. • Activated STAT-3 can promote hyper-inflammation, lung fibrosis and thrombosis. • Activated STAT-3 promotes lymphopenia and impairs anti-virus immune responses. • STAT3 may be a potential therapeutic target for the treatment of COVID-19. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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