Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities DOI Creative Commons

Mingjun Yao,

Zheng Liu, Wei Zhao

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: May 21, 2025

Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease characterized by progressive scarring, alveolar destruction, and limited therapeutic options. Although the exact etiology of IPF remains unclear, emerging evidence suggests that ferroptosis, an iron-dependent form regulated cell death driven lipid peroxidation oxidative stress, plays significant role in its pathogenesis. Ferroptotic stress not only compromises epithelial integrity, but also triggers inflammatory responses profibrotic signaling cascades activate sustain fibroblast dysfunction. This review delineates core regulatory pathways iron metabolism, peroxidation, antioxidant defenses, mitochondrial remodeling, RNA editing, with emphasis on their relevance IPF. We explore how injury macrophage-derived signals initiate subsets, shaped scRNA-seq-defined heterogeneity plasticity, respond to these cues reinforcing ECM deposition stress. Therapeutic avenues targeting including supplementation, chelation, modulation are discussed alongside cell-specific interventions nanodelivery strategies. By integrating recent advances molecular profiling ferroptosis biology, this provides framework for leveraging as tractable target identifies novel directions precision antifibrotic therapy.

Language: Английский

Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities DOI Creative Commons

Mingjun Yao,

Zheng Liu, Wei Zhao

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: May 21, 2025

Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease characterized by progressive scarring, alveolar destruction, and limited therapeutic options. Although the exact etiology of IPF remains unclear, emerging evidence suggests that ferroptosis, an iron-dependent form regulated cell death driven lipid peroxidation oxidative stress, plays significant role in its pathogenesis. Ferroptotic stress not only compromises epithelial integrity, but also triggers inflammatory responses profibrotic signaling cascades activate sustain fibroblast dysfunction. This review delineates core regulatory pathways iron metabolism, peroxidation, antioxidant defenses, mitochondrial remodeling, RNA editing, with emphasis on their relevance IPF. We explore how injury macrophage-derived signals initiate subsets, shaped scRNA-seq-defined heterogeneity plasticity, respond to these cues reinforcing ECM deposition stress. Therapeutic avenues targeting including supplementation, chelation, modulation are discussed alongside cell-specific interventions nanodelivery strategies. By integrating recent advances molecular profiling ferroptosis biology, this provides framework for leveraging as tractable target identifies novel directions precision antifibrotic therapy.

Language: Английский

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