Document Type : Review Article
Laboratory of Physiology, Faculty of Medicine of Tunis, University of Tunis El Manar, La Rabta 1007, Tunis, Tunisia.
Laboratory of Physiopathology, Food and Biomolecules (LR-17-ES-03), Technology Center of Sidi Thabet, University of Manouba, Tunis, Tunisia
Laboratory of Physiology, Faculty of Medicine of Tunis, University of Tunis El Manar, La Rabta 1007, Tunis, Tunisia
Idiopathic Pulmonary Fibrosis (IPF) is a lung disease characterized by formation of fibroblast foci and honeycomb lesions in the pulmonary parenchyma. The physiopathological mechanisms involved in the development of fibrosis and architectural disorganization are still imperfectly elucidated. In fact, lesion formation is irreversible and no treatment, to date, has been shown to be effective (30% of patients die within 5 years of the onset of the disease). The long-held concept of chronic inflammation leading to fibrosis is still controversial. Indeed, recent data suggest that the physiopathology of this disease is the product of fibroblast dysfunction rather than the result of an inflammatory imbalance. This concept supports the parallel involvement of three main factors: epithelial damage, angiogenesis and oxidative stress. In this review we highlighted the different factors and the ethiopathogenic pathways involved in the fibrotic process, in order to increase our understanding of the mechanisms involved in this pulmonary pathology.