Purpose of review
To summarize the new knowledge on tissue remodeling in the context of lung diseases. Tissue remodeling includes changes in cells: differentiation; response to growths factors, hormones, or environmental factors; and composition of the extracellular matrix. So, can one trigger cause them all or are they independently regulated?
New evidence from clinical and experimental studies strengthened the view that a susceptibility to remodeling can be initiated in early life and be re-activated by environmental triggers later in life. Many studies further support the idea that TGF-β plays the central role in the pathogenesis of remodeling and fibrosis. However, the activation pathways and the end-effect of TGF-β activation seems to be distinctive of disease and effecter cell specific patterns. The existing animal models do not properly reflect the human disease and thus have to be further improved.
The central role of TGF-β on pathological mechanisms leading to remodeling and fibrosis has been further confirmed. However, the questions of why TGF-β is activated as well as its disease and cell type specific mode of action remain to be answered. Based on clinical data redefining the term ‘tissue remodeling’ in a disease and cell type specific way should be considered.