Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease.
Stefano SoldanoVanessa SmithPaola MontagnaEmanuele GotelliRosanna CampitielloCarmen PizzorniSabrina PaolinoAlberto SulliAndrea CereMaurizio CutoloPublished in: Arthritis research & therapy (2024)
In cultured MDMs from SSc-ILD pts, nintedanib seems to downregulate the profibrotic M2 phenotype through the significant reduction of gene expression and protein synthesis of M2 cell surface markers, together with the significant reduction of TGFβ1 release, and notably MerTK, a tyrosine kinase receptor involved in lung fibrosis.
Keyphrases
- interstitial lung disease
- systemic sclerosis
- tyrosine kinase
- idiopathic pulmonary fibrosis
- gene expression
- rheumatoid arthritis
- cell surface
- endothelial cells
- end stage renal disease
- epidermal growth factor receptor
- newly diagnosed
- ejection fraction
- chronic kidney disease
- dna methylation
- dendritic cells
- immune response
- transforming growth factor
- epithelial mesenchymal transition
- patient reported outcomes
- liver fibrosis