Since endothelial dysfunction is a risk factor for pulmonary fibrosis (Zhao et al., 2023) and T-cadherin downregulation in COVID-19 patients was associated with dysregulation of endothelial adhesion molecules (Figures 1, 2), we further explored the role of T-cadherin knockout (Cdh13−/−) on angiotensin II-induced endothelial dysfunction in mice. Here, CDH13 is linked to pulmonary fibrosis.