Fig. 1.

Therapeutic targets and potential treatment strategies for COVID-19. SARS-CoV-2 infects airway epithelial cells through interactions with the transmembrane enzyme ACE2. Blocking human ACE2 protein may be a promising therapeutic agent for patients with the virus. Once SARS-CoV-2 enters the cell, the infected cells undergo cell death and release virus particles together with intracellular components, which trigger the inflammatory response. Antiviral agents such as inhibitors of RNA polymerase and protease inhibitors are potential therapeutic strategies. Subsequently, the surge of pro-inflammatory cytokines and dysregulation of the redox balance causes edema and damages capillary and lung tissue, even leading to acute respiratory distress syndrome (ARDS); exacerbation of lung injury also increases the risk of lung fibrosis. Drugs inhibiting the pro-inflammatory cytokines, such as tocilizumab (an inhibitor of IL-6) are recommended in the cytokine storm phase of the disease, and modulators of the redox state may be used to restore the redox balance. When other organs, such as liver, kidney, heart, and spleen, are flooded with inflammatory cytokines and chemokine, organ failure ensues, with fatal consequences. Extracorporeal membrane oxygenation (ECMO) has a role in the treatment of severe COVID-19 at this stage. RBD: receptor-binding domain; TGF: transforming growth factor; ROS: reactive oxygen species; RNS: reactive nitrogen species; ALT: alanine aminotransferase; AST: aspartate transaminase; BUN: blood urea nitrogen; BNP: B-type natriuretic peptide; cTnI: cardiac troponin I; cTnT: cardiac troponin T.