Abstract
PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by progressive destruction of alveolar structures, excessive fibroproliferation, and unrestrained extracellular matrix deposition. Transforming growth factor beta (TGF-β), a profibrotic cytokine aberrantly expressed in IPF lungs, is a potent regulator of fibrogenesis and connective tissue synthesis. We recently reported that pirfenidone binds competitively to the ATP-binding site of two isoforms of p38 MAPK (p38α and p38γ), a key intracellular mediator of TGF-β-induced collagen synthesis. In order to further explore the potential therapeutic utility of pirfenidone in IPF, we sought to confirm the expression of p38γ in human lung fibroblasts and investigate the inhibitory activity of pirfenidone against TGF-β-induced p38α and p38γ activation in these cells.
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