Lysophosphatidylcholine acyltransferase 1 alleviates silica-induced pulmonary fibrosis by modulating lipid metabolism

Downregulation of HMGCS2 mediated AECIIs lipid metabolic alteration promotes pulmonary fibrosis by activating fibroblasts

“…2 A). Based on the KEGG analysis, we hypothesized that LysoPC, which was derived from glycerophospholipid with the substitution of choline [ 10 , 25 ], might be the vital lipid involved in the process of fibrotic progression. To further unveil what specific type of LysoPC species could activate lung fibroblast, we selected the top-ranked LysoPCs with compound ID which were commercialized available (Table S 2 ) and confirmed that LysoPC(14:0) HMDB0010379 and LysoPC (16:0) HMDB0240262 could activated lung fibroblast in vitro (Fig.…”

“…Recent studies showed that metabolism deregulation was a key feature of IPF [ 7 – 9 ], and clinical studies demonstrated that abnormal lipids were detected in the serum and BALF in both IPF patients and experimental mice [ 10 – 12 ]. However, which type of cells contributed to the dysregulated lipid metabolism phenotype remained unknown, and the subsequent biological function and possible mechanisms of altered lipid metabolism in the process of IPF were still undetermined.…”

“…The current paradigm of IPF proposes repeated cycles of injury to lung alveolar epithelial cells, stimulating the recruitment and activation of tissue fibrogenic cells, leading to fibrosis and end-stage organ failure. Recent studies showed that metabolism deregulation was a key feature of IPF [ 7 – 9 ], and clinical studies demonstrated that abnormal lipid was detected in the serum and Bronchoalveolar Lavage Fluid (BALF) in both IPF patients and experimental mice model [ 10 – 12 ]. However, the origin of the lipid remained unknown, and the biological function and possible mechanisms of increased lipid in the process of IPF were still undetermined.…”

From Basic Research to Clinical Practice: Considerations for Treatment Drugs for Silicosis

“…Quercetin reduces the accumulation of myofibroblasts and restores fibroblast apoptosis sensitivity by upregulating the Fas ligand receptor and the expression of caveolin-1 [52]. Dihydroquercetin inhibits ferritin phagocytosis-mediated iron death in cells and improves silica-induced pulmonary fibrosis [49], while lysophosphatidylcholine acyltransferase 1 (LPCAT1) alters the balance between phosphatidylcholine and lysophosphatidylcholine and inhibits the development of silicosis in mice [92].…”

High-Fat Diet Related Lung Fibrosis-Epigenetic Regulation Matters

“…Pulmonary fibrosis (PF) is an interstitial lung disease characterized by inflammation and destruction of lung parenchyma caused by accelerated extra cellular matrix (ECM) deposition [ 1 , 2 ] which impaired gas exchange thus decreased quality of life [ 3 ]. Despite the well-known etiological factors such as senescence and aging, PF is recently recognized as a metabolic disease [ 4 , 5 ] and abnormal lipid signature has been observed both in serum and bronchoalveolar lavage fluid (BALF) of PF patients and mice model suggesting disturbed lipid metabolism [ 6 , 7 , 8 ]. Currently there is no cure for PF except for lung transplantation therefore revealing the potential pathogenic factors and possible mechanisms would contribute to the prevention and treatment of this deadly disease.…”