Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic irreversible interstitial lung disease characterized by a progressive decline in lung function. The etiology of IPF is unknown, which poses a significant challenge to the treatment of IPF. Recent studies have identified a strong association between lipid metabolism and the development of IPF. Qualitative and quantitative analysis of small molecule metabolites using lipidomics reveals that lipid metabolic reprogramming plays a role in the pathogenesis of IPF. Lipids such as fatty acids, cholesterol, arachidonic acid metabolites, and phospholipids are involved in the onset and progression of IPF by inducing endoplasmic reticulum stress, promoting cell apoptosis, and enhancing the expression of pro-fibrotic biomarkers. Therefore, targeting lipid metabolism can provide a promising therapeutic strategy for pulmonary fibrosis. This review focuses on lipid metabolism in the pathogenesis of pulmonary fibrosis.

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