Fibrotic extracellular matrix microenvironment induces alveolar type II epithelial cell senescence via integrin-β1/FAK/YAP signaling pathway.

Jingwen Yang, Yuan Ma, Ran Zhang, Xiangyi Liu, Wenjing Liu, Chen Liu, Jiangan Guan, Wenwen Chen, Jie Weng, Mengying Xie, Zhibin Wang, Xinlong Wan, Zhiyi Wang, Chan Chen

Department of Geriatric Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China; Wenzhou Key Laboratory of Precision General Practice and Health Management, Wenzhou 325027, China.Department of Geriatric Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China; Wenzhou Key Laboratory of Precision General Practice and Health Management, Wenzhou 325027, China. · pubmed

Paper

Abstract

Senescent alveolar epithelial cells (AEC) play a pivotal role in the progression of idiopathic pulmonary fibrosis (IPF), attracting increasing attention from researchers. Central to the pathogenesis of pulmonary fibrosis (PF) is the excessive deposition of extracellular matrix (ECM). However, there remains a significant gap in understanding how the ECM microenvironment influences senescence in type II alveolar epithelial cells (AEC II). This study investigates the activation of the integrin-β

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Research summary

The paper claims that the fibrotic extracellular matrix microenvironment induces senescence in alveolar type II epithelial cells via the integrin-β1/FAK/YAP signaling pathway. This research is relevant as it explores the mechanisms underlying cellular senescence, which is a key factor in aging and age-related diseases like pulmonary fibrosis.

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