New evidence for T-cadherin in COVID-19 pathogenesis, endothelial dysfunction, and lung fibrosis.

ABSTRACT: The COVID-19 pandemic had an unprecedented impact on all aspects of human activity worldwide, frequently resulting in post-acute sequelae and affecting multiple organ systems. The underlying mechanisms driving both acute and post-acute manifestations of COVID-19 are still poorly understood, warranting further investigation for new targets. The study represents the first attempt to explore the role of T-cadherin in COVID-19 pathogenesis as well as its implications in pulmonary fibrosis and endothelial dysfunction. First, we revealed a significant decrease in T-cadherin expression in post-mortem lung samples from COVID-19 patients. This downregulated T-cadherin expression correlated with the elevated levels of VE-cadherin and reduced levels of β-catenin, suggesting a disruption in endothelia

SUBMITTER: Semina E 

PROVIDER: S-EPMC11920143 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature