Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms

Caveolin is a structural protein of flask-shaped invaginations of the plasma membrane termed as caveolae and is widely expressed on the endothelial cells, smooth muscle cells and fibroblasts in the different parts of the body including the lung tissues. The expression of caveolin-1 in the lung tissues is important to prevent the fibrogenic actions of TGF-β1 in lung fibrosis of different etiology including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease and allergen-induced airway remodeling. Caveolin-1-mediated internalization and degradation of TGF-β1 receptors may possibly account for the decreased actions of TGF-β1. Studies have shown that the deficiency of caveolin-1 is very important in inducing lung fibrosis and its upregulation is reported to prevent lung fibrosis. The biological actions of caveolin-1 involve signaling pathways including JNK signaling, IL-4, STAT-3, miR199a-5p, CXCR4+ and CXCL12. The present review discusses the key role of caveolin and associated signaling pathways in the pathogenesis of lung fibrosis of different etiology.