Histochemistry and cell biologySep 11, 2026

How lung cell connections contribute to early lung damage and scarring from COVID-19

Long Covid Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Sep 12, 2026

Abstract

p120 catenin abundance was higher in chronic COVID-19 compared with acute COVID-19.

Increased p120 catenin levels may suggest its involvement in the progression of pulmonary fibrosis associated with COVID-19.
Caveolin-1 and P2X7R proteins were found to be decreased in COVID-19 lungs, indicating a potential role in the early stages of the disease.
Early lung injury models did not show changes in p120 catenin or its phosphorylated form in cell culture, suggesting complexity in its regulatory mechanisms.
A reduction of p120 catenin was noted in murine lung cultures, which may relate to fibrotic processes.
Alterations in p120 catenin and its interacting proteins could contribute to the development of pulmonary fibrosis following COVID-19.

Simplified

Pulmonary fibrosis is a chronic progressive disease, caused by numerous factors, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Damage to the alveolar epithelial barrier (formed by junctions between alveolar epithelial cells I) has been described as a key mechanism of early fibrosis and therefore could be crucial for COVID-19-associated sequelae. The integrity of adherens junctions is regulated by p120 catenin and is crucial for barrier regulation in epithelial-mesenchymal-transition-driven diseases such as fibrogenesis and cancer. Abundance and expression of p120 catenin and intercellular contact regulating proteins (caveolin-1, P2X7R) were investigated retrospectively in COVID-19 lungs (acute, chronic) compared with healthy controls and interstitial lung disease of different etiologies (n = 6). p120 Catenin was further investigated in early injury models using profibrotic agents in murine lung and human alveolar epithelial cell culture. p120 Catenin abundance was higher in chronic COVID-19 compared with acute COVID-19, suggesting a role in fibrotic development. The interacting proteins caveolin-1 and P2X7R were simultaneously decreased in COVID-19, indicating a role in early pathophysiology. Early epithelial damage showed no changes in p120 catenin and its phospho-Y228 site in cell culture whereas p120 catenin was reduced in murine lung culture. Thus, alterations in and interactions between p120 catenin and caveolae associated proteins may represent a potential mechanism underlying COVID-19-induced pulmonary fibrosis.

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How lung cell connections contribute to early lung damage and scarring from COVID-19

Abstract

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