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Description

10.3389/fnagi.2017.00068 222 PimentelL

Inflammatory cytokines: Methyl palmitate is a promising drug that inhibits macrophage activation, reduces TNF- level and reduces fibrosis ( Recruitment: Nintedanib is an existing triple kinase inhibitor that has inhibitory action on CSF-1R as well and blocks M2 polarisation ( Signalling pathways: Tacrolimus, Ruxolitinib inhibit the JAK/STAT pathways supressing the profibrotic M2 pathway ( Fibroblast activation: Traditional Chinese medicine like Schisandra chinensis and Resveratrol have anti-TGF- activity and hold excellent potential ( Macrophage apoptosis: BCL-2 inhibitors promote apoptosis and have demonstrated resolution of fibrosis in mice ( Discussion The first step in the development of lung fibrosis in most autoimmune diseases is damage of alveolar epithelium and inflammation followed by continuous TGF- signalling resulting in epithelial to mesenchymal transformation ( H17 differentiation, impaired autophagy and apoptosis to activation of profibrotic pathways