What question did this study set out to answer?

To determine how cadherin-11 regulates type II alveolar epithelial cell injury and mesenchymal gene expression during the pathogenesis of pulmonary fibrosis.

September 18, 2026AJP Cell PhysiologyOpen Access

Cadherin-11 Regulation of Type II Alveolar Epithelial Cells During Pulmonary Fibrosis

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Authors

MPMesias Pedroza STSarah To JSJennifer Smith

Discussion

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Overview

Preclinical study demonstrates that Cadherin-11 drives type II alveolar epithelial cell injury during pulmonary fibrosis, indicating a potential target for therapeutic intervention.

Key Points

To determine how cadherin-11 regulates type II alveolar epithelial cell injury and mesenchymal gene expression during the pathogenesis of pulmonary fibrosis.
Quantified Cadherin-11 (CDH11) expression in lung samples from patients with idiopathic pulmonary fibrosis and healthy controls, correlating expression levels with pulmonary function.
Evaluated pulmonary fibrosis using an intraperitoneal bleomycin model in wild-type mice, global Cdh11-deficient mice, and mice treated with CDH11-neutralizing monoclonal antibodies.
Characterized cell-specific mechanisms using alveolar type II cell-selective deletion mice (Cdh11 floxed-SPC-Cre) and in vitro cadherin engagement assays assessing transitional and mesenchymal markers.
CDH11 expression was significantly elevated in idiopathic pulmonary fibrosis lung tissue compared to controls and was inversely correlated with lung function.
Global genetic deletion or monoclonal antibody blockade of CDH11 reduced bleomycin-induced pulmonary fibrosis and lowered epithelial injury and mesenchymal marker expression.
CDH11 co-localized with alpha-SMA and KRT8 in injured alveolar type II cells, and selective deletion of Cdh11 in these cells significantly attenuated pulmonary fibrosis in vivo.

Cite This Study

Pedroza et al. (2026) studied this question.

synapsesocial.com/papers/6aad0bb6de0393d728b8a238 https://doi.org/10.1152/ajpcell.00164.2026

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September 18, 2026AJP Cell PhysiologyOpen Access

Cadherin-11 Regulation of Type II Alveolar Epithelial Cells During Pulmonary Fibrosis

View Full Paper

Ask AI

Bookmark

Authors

MPMesias Pedroza STSarah To JSJennifer Smith

Discussion

Member takes

Overview

Preclinical study demonstrates that Cadherin-11 drives type II alveolar epithelial cell injury during pulmonary fibrosis, indicating a potential target for therapeutic intervention.

Key Points

To determine how cadherin-11 regulates type II alveolar epithelial cell injury and mesenchymal gene expression during the pathogenesis of pulmonary fibrosis.
Quantified Cadherin-11 (CDH11) expression in lung samples from patients with idiopathic pulmonary fibrosis and healthy controls, correlating expression levels with pulmonary function.
Evaluated pulmonary fibrosis using an intraperitoneal bleomycin model in wild-type mice, global Cdh11-deficient mice, and mice treated with CDH11-neutralizing monoclonal antibodies.
Characterized cell-specific mechanisms using alveolar type II cell-selective deletion mice (Cdh11 floxed-SPC-Cre) and in vitro cadherin engagement assays assessing transitional and mesenchymal markers.
CDH11 expression was significantly elevated in idiopathic pulmonary fibrosis lung tissue compared to controls and was inversely correlated with lung function.
Global genetic deletion or monoclonal antibody blockade of CDH11 reduced bleomycin-induced pulmonary fibrosis and lowered epithelial injury and mesenchymal marker expression.
CDH11 co-localized with alpha-SMA and KRT8 in injured alveolar type II cells, and selective deletion of Cdh11 in these cells significantly attenuated pulmonary fibrosis in vivo.

Cite This Study

Pedroza et al. (2026) studied this question.

synapsesocial.com/papers/6aad0bb6de0393d728b8a238 https://doi.org/10.1152/ajpcell.00164.2026

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