Cx3cr1 depletion ameliorates lipid metabolic dysregulation and pulmonary fibrosis induced by silica - PubMed
5 hours ago
- #silicosis
- #lipid metabolism
- #pulmonary fibrosis
- Silicosis is characterized by pulmonary fibrosis with no effective treatment currently available.
- Dysregulation of macrophage lipid metabolism plays a critical role in pulmonary fibrosis pathogenesis.
- Cx3cr1 is identified as a key gene in lung macrophage lipid metabolism in a silicosis murine model.
- Cx3cr1 depletion ameliorates silica-induced pulmonary fibrosis by inhibiting lipid metabolic dysregulation.
- Transcriptomic and flow cytometry analyses identified Cx3cr1+ macrophages as key regulators in silicosis fibrosis.
- Single-cell RNA sequencing confirmed Cx3cr1's role in lung macrophage lipid metabolism in bleomycin-induced fibrosis.
- Cx3cr1 knockout reduces lipid accumulation, pro-inflammatory mediators, and pulmonary fibrosis in vivo.
- In vitro studies with RAW264.7 cells and BMDMs showed Cx3cr1 depletion improves lipid metabolic regulation.
- Mendelian Randomization analysis identified CX3CR1 as a risk factor for pneumoconiosis.
- Targeted inhibition of Cx3cr1 may offer a therapeutic approach for silicosis and related fibrosis.