Fig. 8: Evaluation of lnc668 as a therapeutic target for pulmonary fibrosis.

a lnc668 interference fragment and overexpression adenoviral vector were administered to mice via intratracheal injection. b Body weight loss was obvious in the BLM and lnc668 overexpression groups. The si-lnc668 group did not experience remarkable weight loss. c Lung function in the si-lnc668 group improved compared with that in the BLM group. Similar to BLM treatment, lnc668 overexpression decreased lung function. d Total lung capacity after si-lnc668 treatment increased compared with that after BLM treatment. Similar to BLM treatment, lnc668 overexpression decreased total lung capacity. e MicroCT imaging system for small animals revealed that interfering with lnc668 alleviated the pulmonary fibrosis caused by BLM. lnc668 overexpression accelerated pulmonary fibrosis. f HE and Masson staining demonstrated that alveolar walls thickened, alveolar structures became disordered, and collagen deposition increased in the BLM model group. si-lnc668 attenuated the above symptoms. lnc668 overexpression caused symptoms similar to those caused by BLM treatment. g Western blot confirmed that compared with BLM treatment, interference with lnc668 reduced the expression levels of FAP, α-SMA, COL1A, COL3A, and VIM. lnc668 overexpression increased the expression levels of these proteins. h lnc668 expression in the blood of patients with IPF was significantly higher than that in healthy individuals. i qRT-PCR proved that lnc668 expression in the blood of normal people increased with the increase in age.