Recovery from ARDS is possible but only before the disease progresses to a critical stage. However, a mortality rate between 35 and 40% in ARDS patients demonstrates irreversible tissue damage manifested by tissue fibrosis (Bellani et al., 2016). TGF-β plays a central role in the late onset of fibrotic changes during ARDS. Acting with other proinflammatory molecules, TGF-β induces fibroblast cell proliferation and activation, collagen synthesis and deposition, synthesis of fibronectin, and alpha-smooth muscle actin, which all together contribute to fibrosis (Fan E. et al., 2020). Emerging histological studies from deceased COVID-19 patients reveal robust structural changes in the lungs and associated organs like the liver, kidneys, and heart (George et al., 2020). Lung biopsy samples from a 50-year-old patient who had succumbed to COVID-19 revealed hyaline membrane formation, desquamation of epithelial and endothelial cells, mononuclear infiltration, and robust ATII cell damage, indicating ARDS (Xu Z. et al., 2020).