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?:abstract
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The 2019 novel coronavirus (2019-nCoV) is still spreading rapidly around the world, and one cause of lethality for patients infected with 2019-nCoV is acute respiratory distress syndrome (ARDS). ARDS is a severe syndrome of acute lung injury (ALI) that is predominantly triggered by inflammation and results in a sudden loss of, or damage to, kidney function. Emerging studies reveal that multiple transcription factor-associated signaling pathways are activated in the pathology of ALI/ARDS. Of these pathways, the activation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), AP-1 (activator protein 1), IRFs (interferon regulatory factors), STATs (signal transducer and activator of transcription), Wnt/β-catenin-TCF/LEF (T-cell factor/lymphoid enhancer-binding factor), and CtBP2 (C-Terminal binding protein 2)-associated transcriptional complex contributes to ALI/ARDS pathology through diverse mechanisms, such as inducing proinflammatory cytokine levels and mediating macrophage polarization. In this review, we present an updated summary of the mechanisms underlying these signaling activations and regulations, as well as their contribution to the pathogenesis of ALI/ARDS. We aim to develop a better understanding of how ALI/ARDS occurs and improve ALI/ARDS therapy.
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