Research Progress on the Regulatory Role of Ferroptosis in the Progression of Idiopathic Pulmonary Fibrosis

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease with unknown etiology, rapid progression and extremely poor prognosis. Its core pathological manifestations include usual interstitial pneumonia lesions in lung tissue, abnormal proliferation of fibroblasts and excessive deposition of extracellular matrix (ECM). The median survival time of patients after diagnosis is only 2–3 years, and there is still no radical cure at present. Ferroptosis is a novel iron-dependent programmed cell death driven by lipid peroxidation, which is fundamentally different from traditional cell death modes such as apoptosis and autophagy. Its core biological characteristics include intracellular iron overload, massive accumulation of lipid reactive oxygen species (lipid ROS), and functional failure of antioxidant defense systems. In recent years, accumulating studies have confirmed that ferroptosis exerts a pivotal regulatory role in the initiation and progression of IPF by modulating iron metabolic homeostasis, lipid peroxidation and intercellular signal crosstalk. This paper systematically reviews the core regulatory network of ferroptosis, cell-specific regulatory mechanisms of ferroptosis during IPF progression, research breakthroughs of related biomarkers, and advances in targeted ferroptosis therapeutic strategies, aiming to provide novel theoretical basis and research directions for the investigation of IPF pathogenesis and clinical precision treatment.