High-Fat Diet Related Lung Fibrosis-Epigenetic Regulation Matters

Pulmonary fibrosis (PF) is an interstitial lung disease characterized by the destruction of the pulmonary parenchyma caused by excessive extracellular matrix deposition. Despite the well-known etiological factors such as senescence, aberrant epithelial cell and fibroblast activation, and chronic inflammation, PF has recently been recognized as a metabolic disease and abnormal lipid signature was observed both in serum and bronchoalveolar lavage fluid (BALF) of PF patients and mice PF model. Clinically, observational studies suggest a significant link between high-fat diet (HFD) and PF as manifested by high intake of saturated fatty acids (SFAs) and meat increases the risk of PF and mice lung fibrosis. However, the possible mechanisms between HFD and PF remain unclear. In the current review we emphasize the diversity effects of the epigenetic dysregulation induced by HFD on the fibrotic factors such as epithelial cell injury, abnormal fibroblast activation and chronic inflammation. Finally, we discuss the potential ways for patients to improve their conditions and emphasize the prospect of targeted therapy based on epigenetic regulation for scientific researchers or drug developers.

Automated summary

Pulmonary fibrosis is a metabolic disease characterized by excessive extracellular matrix deposition, and abnormal lipids have been observed in PF patients and mice models. High-fat diet, particularly the intake of saturated fatty acids and meat, is significantly associated with PF and lung fibrosis. However, the mechanisms underlying the connection between high-fat diet and PF are still unclear. This review highlights the diverse effects of epigenetic dysregulation induced by high-fat diet on fibrotic factors and discusses potential ways to improve patients' conditions and the prospect of targeted therapy based on epigenetic regulation.