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. Author manuscript; available in PMC: 2021 Apr 1.
Published in final edited form as: J Cell Physiol. 2021 Feb 24;236(9):6597–6606. doi: 10.1002/jcp.30343

Figure 5. Schematic representation of the potential effects of HMGB1, hyperglycemia, and TCBN on ACE2 expression and SARS-CoV2 binding to lung epithelial cells.

Figure 5.

(A) HMGB1 or high glucose-induced AGE (advanced glycation end-products) promotes the expression of ACE2 receptors thereby increasing the risk of SARS-CoV-2 interaction with the lung epithelial cell surface ACE2 leading to their internalization and infection. (B) Whereas Akt inhibitor MK-2206 does not affect the expression of ACE2 receptors, treatment with TCBN blunts HMGB1 and hyperglycemia-induced ACE2 expression in lung epithelial cells potentially in an Akt-independent but adenosine-receptor dependent mechanism.