Pulmonary fibrosis: Cellular and molecular events
Mohammed S. Razzaque
Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts, USA and
Department of Pathology, Nagasaki University Graduate School of Medical Sciences, Nagasaki, Japan
Search for more papers by this authorTakashi Taguchi
Department of Pathology, Nagasaki University Graduate School of Medical Sciences, Nagasaki, Japan
Search for more papers by this authorMohammed S. Razzaque
Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts, USA and
Department of Pathology, Nagasaki University Graduate School of Medical Sciences, Nagasaki, Japan
Search for more papers by this authorTakashi Taguchi
Department of Pathology, Nagasaki University Graduate School of Medical Sciences, Nagasaki, Japan
Search for more papers by this authorAbstract
Connective tissue remodeling of the interstitium is an important feature of chronic lung diseases encompassing interstitial inflammatory changes and subsequent pulmonary fibrosis. The early inflammatory phase is usually associated with the release of several cytokines and chemokines by activated resident cells and infiltrating cells which, in turn, help further recruit inflammatory mononuclear cells. Cytokines and growth factors secreted by inflammatory cells and by interstitial cells (fibroblasts and myofibroblasts) play an important role in the fibrogenic phase of pulmonary fibrosis by inducing matrix synthesis. In addition, matrix-degrading enzymes and their inhibitors also contribute to extracellular matrix (ECM) remodeling in pulmonary fibrosis. This review addresses the pathophysiology of wound healing and different phases of pulmonary fibrosis.
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