A Two Pronged Weapon in the Fight Against Fibrosis. Focus On "Inhibition of Wnt/Β-Catenin Signaling Promotes Epithelial Differentiation of Mesenchymal Stem Cells and Repairs Bleomycin-Induced Lung Injury"
"PULMONARY FIBROSIS was first described in the 1930s, and while its etiology has become somewhat more clear in recent years, the disease remains virtually untreatable (1, 5). The etiology of pulmonary fibrosis has stirred considerable debate over the years. Initially, pulmonary fibrosis was treated as an inflammatory disease. However, poor clinical response to anti-in- flammatory therapy made evident that the inflammatory responses seen in histological examination of biopsied fibrotic tissue are 'paraphenomena' (4). The more contemporary hypothesis is that progression of pulmonary fibrosis is due to defects in organ repair processes and/or alterations in the intricate cell-cell signaling events that mediate normal wound healing (3, 10). While debates have raged over the pathogenesis of pulmonary fibrosis, all have agreed that new therapeutic approaches, preferably ones that target multiple aspects of the disease, are clearly needed."
Rennolds S Ostrom. A two pronged weapon in the fight against fibrosis, Focus on "Inhibition of Wnt/β-Catenin Signaling Promotes Epithelial Differentiation of Mesenchymal Stem Cells and Repairs Bleomycin-induced Lung Injury." Am J Physiol, Cell Physiol, 307(3):C232-3, 2014.
American Physiological Society