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AMD3100 effectively reduced CXCR4 and CXCL12 expression in the silicotic lung. (A and B) Representative images show CXCR4 (upper) and CXCL12 (bottom) expression in lung sections determined by immunohistochemical staining analysis on day 28. Red arrows indicate CXCR4 + cells. Green arrows indicate CXCL12 + cells. DAB-labeled tissues were analyzed using Image-Pro Plus 6.0 software, as described in the material and methods. IOD: integrated optical density. Scale bar: 100 μm. (C) The expression of CXCR4 in the lungs was analyzed by Western blot on day 7. N=3 per group. **p < 0.01, ***p < 0.001 vs the control group. # P < 0.05, ## P < 0.01 vs the CS group.
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Background
Silicosis is a severe pulmonary disease caused by inhaling dust containing crystalline silica. The progression of silicosis to pulmonary fibrosis is usually unavoidable. Recent studies have revealed positivity for the overexpression of C-X-C chemokine receptor type 4 (CXCR4) in pulmonary fibrosis and shown that the CXCR4 inhibitor AMD310...
Citations
Inflammation is the body's defense response to exogenous or endogenous stimuli, involving complex regulatory mechanisms. Discovering anti‐inflammatory drugs with both effectiveness and long‐term use safety is still the direction of researchers' efforts. The inflammatory pathway was initially identified to be involved in tumor metastasis and HIV infection. However, research in recent years has proved that the CXC chemokine receptor type 4 (CXCR4)/CXC motif chemokine ligand 12 (CXCL12) axis plays a critical role in the upstream of the inflammatory pathway due to its chemotaxis to inflammatory cells. Blocking the chemotaxis of inflammatory cells by CXCL12 at the inflammatory site may block and alleviate the inflammatory response. Therefore, developing CXCR4 antagonists has become a novel strategy for anti‐inflammatory therapy. This review aimed to systematically summarize and analyze the mechanisms of action of the CXCR4/CXCL12 axis in more than 20 inflammatory diseases, highlighting its crucial role in inflammation. Additionally, the anti‐inflammatory activities of CXCR4 antagonists were discussed. The findings might help generate new perspectives for developing anti‐inflammatory drugs targeting the CXCR4/CXCL12 axis.
