Abstract
Fatty acid metabolism, including the de novo synthesis, uptake, oxidation, and derivation of fatty acids, plays several important roles at cellular and organ levels. Recent studies have identified characteristic changes in fatty acid metabolism in idiopathic pulmonary fibrosis (IPF) lungs, which implicates its dysregulation in the pathogenesis of this disorder. Here, we review the evidence for how fatty acid metabolism contributes to the development of pulmonary fibrosis, focusing on the profibrotic processes associated with specific types of lung cells, including epithelial cells, macrophages, and fibroblasts. We also summarize the potential therapeutics that target this metabolic pathway in treating IPF.
Highlights
Idiopathic pulmonary fibrosis (IPF) is a fatal fibrotic disorder of unknown etiology
We describe the general concepts in fatty acid (FA) metabolism and the pathology of IPF
Various FA metabolism pathways are intricately intertwined, and a perturbation of any of these in the lung may contribute to the development of pro-fibrotic phenotypes in epithelial cells, macrophages, and fibroblasts/myofibroblasts (Figure 2)
Summary
Idiopathic pulmonary fibrosis (IPF) is a fatal fibrotic disorder of unknown etiology. Mechanistic features include epithelial apoptosis, macrophages releasing pro-fibrotic mediators, and the activation of fibroblasts and myofibroblasts. We analyze the roles of this metabolic pathway in regulating the function of specific cells and the relevant pathologic cellular responses in IPF, including pro-fibrotic phenotype changes of alveolar epithelial cells and macrophages, and fibroblast/myofibroblast activation.
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