Alveolar epithelial cell dysfunction and epithelial-mesenchymal transition in pulmonary fibrosis pathogenesis DOI Creative Commons

Caopei Zheng,

Ling Zhang, Yuqing Sun

и другие.

Frontiers in Molecular Biosciences, Год журнала: 2025, Номер 12

Опубликована: Апрель 24, 2025

Pulmonary fibrosis (PF) is a progressive and lethal interstitial lung disease characterized by aberrant scar formation destruction of alveolar architecture. Dysfunctional epithelial cells (AECs) play central role in initiating PF, where chronic injury triggers apoptosis disrupts homeostasis, leading to epithelial-mesenchymal transition (EMT). This dynamic reprogramming process causes AECs shed markers adopt mesenchymal phenotype, fueling fibroblast activation pathological extracellular matrix (ECM) deposition. review systematically explores the multi-layered mechanisms driving dysfunction EMT, focusing on core signaling axes such as transforming growth factor-β (TGF-β)/Smad, WNT/β-catenin, NF-κB-BRD4, nuclear factor erythroid 2-related 2 (Nrf2), which regulate EMT fibroblast-ECM interactions. It also highlights emerging regulators, including metabolic reprogramming, exosomal miRNA trafficking, immune-epithelial Furthermore, understanding these essential for developing targeted therapeutic strategies modulate pathways halt or reverse progression, offering critical insights into potential clinical treatments PF.

Язык: Английский

Alveolar epithelial cell dysfunction and epithelial-mesenchymal transition in pulmonary fibrosis pathogenesis DOI Creative Commons

Caopei Zheng,

Ling Zhang, Yuqing Sun

и другие.

Frontiers in Molecular Biosciences, Год журнала: 2025, Номер 12

Опубликована: Апрель 24, 2025

Pulmonary fibrosis (PF) is a progressive and lethal interstitial lung disease characterized by aberrant scar formation destruction of alveolar architecture. Dysfunctional epithelial cells (AECs) play central role in initiating PF, where chronic injury triggers apoptosis disrupts homeostasis, leading to epithelial-mesenchymal transition (EMT). This dynamic reprogramming process causes AECs shed markers adopt mesenchymal phenotype, fueling fibroblast activation pathological extracellular matrix (ECM) deposition. review systematically explores the multi-layered mechanisms driving dysfunction EMT, focusing on core signaling axes such as transforming growth factor-β (TGF-β)/Smad, WNT/β-catenin, NF-κB-BRD4, nuclear factor erythroid 2-related 2 (Nrf2), which regulate EMT fibroblast-ECM interactions. It also highlights emerging regulators, including metabolic reprogramming, exosomal miRNA trafficking, immune-epithelial Furthermore, understanding these essential for developing targeted therapeutic strategies modulate pathways halt or reverse progression, offering critical insights into potential clinical treatments PF.

Язык: Английский

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