Research on Alveolar Type II Epithelial Cell Senescence in Idiopathic Pulmonary Fibrosis
Lichun Zhong1,#, Dijia Wu2,#, Sirui Zhang2, Wenjing Liu2, Faping Wang3,*, Fengming Luo3,*
BIOCELL, Vol.50, No.9, 2026, DOI:10.32604/biocell.2026.078898
- 26 August 2026
(This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)
Abstract Idiopathic pulmonary fibrosis (IPF) is an age-associated, progressive fibrotic interstitial lung disease with limited disease-modifying therapies and poor long-term outcomes. Increasing evidence indicates that senescence of alveolar type II epithelial (AT2) cells is not merely a bystander phenomenon but a central driver of epithelial dysfunction, failed alveolar regeneration, and fibrotic remodeling. In this narrative review, we summarize recent mechanistic, single-cell, epigenetic, and translational studies that have reshaped the epithelial-centered model of IPF. We first outline normal AT2 biology and the regenerative AT2-to-AT1 trajectory, and then discuss how telomere dysfunction, endoplasmic reticulum stress, mitochondrial injury, DNA More >