Fibrosing lung diseases (FLD) are a serious problem to health and are ranked high among chronic degenerative diseases due to its morbidity. The factors triggering the development of FLD are known. Immunological, genetic and/or viral components may be present. Structural alterations of these pathologies consist in the thickening of lung interstitia generally by sharp deposition of extracellular matrix. Bronchi, epithelial and endothelial cells, alveolar septa and pulmonary vascular network are affected. All FLDs remodel the lung architecture, affect different structures and determine qualitative and quantitative functional changes. In the present paper we have raised the hypothesis that different mechanisms of pulmonary lesion occur in experimental models of fibrosing diseases induced by bleomycin and paraquat, which enables us to establish the remodeling process closer to the human pulmonary fibrosis. The study and comprehension of the mechanisms linked with the increase in collagen fibers, in the cells intervening in their production and in the functional analysis of pulmonary fibrosis mechanisms can contribute to understanding these fibrotic pulmonary diseases' pathogenesis.
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