Therapeutic Potential of Mesenchymal Stem Cells and Their Secretome in the Treatment of SARS-CoV-2-Induced Acute Respiratory Distress Syndrome

Figure 1

Cellular entry of SARS-CoV-2. Envelope, membrane, and spike proteins form the SARS-CoV-2 protein interface to the external environment. After inhalation, aerosols containing SARS-CoV-2 penetrate the depths of the lungs and cause severe pneumonia, alveolar injury, and acute respiratory distress syndrome (ARDS). The initial step in the development of SARS-CoV-2-induced ARDS is the interactions between the SARS-CoV-2 spike protein and angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) of alveolar type II cells. TMPRSS2 splits the spike protein into two functional subunits, S1 which interacts with ACE2 and S2 that is further cleaved and activated by TMPRSS2. This structural and conformational change in the spike protein facilitates fusion of viral envelope with the cell membrane of AT2 cells, enabling endocytic entry of the virus in the target cell.