Molecular pathogenesis of emphysema
J. Clin. Invest. Laimute Taraseviciene-Stewart, et al. 118:394 doi:10.1172/JCI31811 [Go to this article.]

Figure 3
Proteolytic destruction of the elastin fiber network by cigarette smoke–activated inflammatory cells. This schematic illustrates the dense elastin fiber network in the lung; the elastin fibers form a particularly dense network around lung capillaries. Neutrophils, macrophages, and dendritic cells have been recognized as producers of proteases. In addition to neutrophil elastase and MMP-12, there have been a myriad of proteases identified in human and animal emphysema that can degrade elastin, collagen, and fibronectin. Loss of the alveolar septal scaffold after enzymatic degradation of various matrix proteins causes airspace enlargement. Elastin peptides are chemotactic and can attract additional inflammatory cells into the lung, thus generating a vicious cycle.