2.6 pulmonary fibrosis
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease mainly occurs in the elderly. It has a poor prognosis, a high mortality rate, and prone to acute exacerbation to respiratory failure[109]. Its etiology is still unknown, however, is frequently associated with smoking, occupational exposure, air pollution, and infection. Damage and repair of alveolar epithelial cells owing to numerous causes, activation of fibroblasts, stimulation of fibropathic proliferation, recruitment and proliferation of immune cells such as alveolar macrophages and lymphocytes, and modulation of the fibrotic response [110], gradual destruction of the normal structure of the lung, and progressive decompensation of lung function IPF can’t be reversed or stopped once it starts, although a number of medications now used to treat it can only slow its advancement[111].
The epithelial-mesenchymal transition (EMT) is critical in the advancement of pulmonary fibrosis since epithelial cells able to de-differentiate then differentiate into mesenchymal cells, which continually produce and accumulate extracellular matrix, directly tied to signaling pathways such as TGF-1, Smad, and ERK/MAP [112]. Silicosis is caused by long-term silica inhalation and deposition in the lungs, which leads to diffuse pulmonary fibrosis. Macrophages are prompted to release TGF-1, which causes lnc ATB expression in epithelial cells and binds to miR-200c to increase ZEB1 expression in silica-induced silicosis pulmonary fibrosis [113]. In addition, miR-29b-2-5p and miR-34c-3p are targets for sponging binding downstream of lnc ATB, upregulating the expression of MEKK2 and NOTCH2, enabling lnc ATB to contribute to the acceleration of the EMT process [114]. Lung epithelial cells express more proliferation and EMT-related genes when lnc NEAT1 interacts with miR-29c [115]. lnc RFAL binds to miR-18a and activates fibroblasts via CTGF to accelerate the process of lung fibrosis [116], lnc RFAL also suppresses miR-26a expression, therefore inhibiting miR-26a’s anti-fibrotic action. A mutually inhibitory feedback loop established between miR-26a and Smad2, leads lnc PFRL to increase fibroblast proliferation and transform into myofibroblast [117].
Liu et al.  reported that in silica-induced lung fibrosis in mice fibroblasts, the overexpression of lnc PCAT29 elevated miR-221 expression, inhibited TGF-β1 in lung fibroblasts, and slowed the lung fibrosis process through the RASAL1/ERK1/2 signaling pathway [118].Through the miR-326/SP1 axis, lnc SNHG1 enhances fibroblast migration, invasion, and fibrogenic molecule production [119], whereas lnc SHNG6 promotes fibroblast activation and collagen accumulation via the miR-26a-5p/TGF-1-smads axis, inducing lung fibrosis in mice [120].