Moisés Selman

Role of matrix metalloproteases in pulmonary fibrosis

Lung fibrosis is the final result of a large variety of stimuli including systemic and autoimmune reactions, exposure to organic and inorganic particles, drugs, and radiation. Independent of etiology, the fibrotic response in the lung can be visualized as a dynamic and highly integrated cellular response to persistent injury and may be related to a damage-triggered inflammatory response or to an aberrant epithelial or endothelial reaction. In any case, the key cellular mediator is the myofibroblast, which when activated is the major effector of the lung remodeling. Several matrix metalloproteases (MMPs) have been shown to participate in this pathological process. These enzymes play an essential but complex role in several interrelated processes that take place in the pathogenesis of lung fibrosis including extracellular matrix remodeling, basement membrane disruption, epithelial apoptosis, cell migration, and angiogenesis. This review will focus on the role of MMPs in the development of lung fibrosis.