Pulmonary Fibrosis; Risk Factors and Molecular Triggers, Insight for Neo Therapeutic Approach

Abstract

Overactivation of the local pulmonary fibroblast induces hyperproduction of the extracellular matrix. A myriad of pathomorphological changes occur during lung fibrosis, including interalveolar space (interstitial) deposition due to proliferation and differentiation of resident fibroblasts, recruitment of circulating stem cells and epithelial–mesenchymal transition, highly reactive and hyperplastic alveolar epithelium. Currently, many endogenous and exogenous factors are believed to be associated with lung fibrosis development. However, pathogenetic treatment remains in the womb of development. Exploring the underlying pathophysiology is crucial for successful development of pathogenetic treatment. Several molecules termed chemokines and cytokines have been found to induce lung fibrosis, such as IL-6, IL-1β, PDGFRα, TNF-α, GM-CSF, and IL-13. However, many others, such as IL-8, RANTES, IP-10, and MIG or lymphotactin, have an antifibrosis effect. However, the pathogenesis is multifactorial and involves dysregulation of the immune system, impaired cell-cell adhesion regulation mechanisms, and loss of DNA repair. The paper aimed to thoroughly addresses the potential risk factors and molecular triggers of lung fibrosis.