Silica-induced telomere dysfunction promotes pulmonary fibrosis through the activation of the cGAS-STING pathway.

Qiuqian Qian, Simiao Pan, Xiaodong Li, Xiaoxue Gong, Zhaoqiang Jiang, Xing Zhang, Jianlin Lou, Lingfang Feng

School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China.School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China. · pubmed

Paper

Abstract

This study aims to elucidate whether silica (SiO₂) induces alveolar epithelial cell senescence through telomere shortening, and to explore the involvement of TERF1 and its subsequent activation of the cGAS-STING pathway in the development of pulmonary fibrosis.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

Silica exposure induces telomere dysfunction in alveolar epithelial cells, contributing to pulmonary fibrosis via the cGAS-STING pathway. The study addresses telomere shortening, a key aspect of cellular aging, and its role in a specific age-related disease, thereby linking environmental factors to mechanisms of aging.

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