Abstract: Abstract: Objective　To explore the interaction between the role of circ_0007762 and miR-18a-5p changes in lung fibroblasts. Methods　Bioinformatics was used to analyze the expression of circ_0007762 in patients with idiopathic pulmonary fibrosis (IPF) and screen its miRNA targets. Circ_0007762 level was verified in HFL1 cells with transforming growth factor (TGF)-β1 intervention. The luciferase activity after co-transfection of miR-18a-5p mimics with reporter gene vectors was verified by dual luciferase reporter assay. CCK8 assay was used to detect the cell viability after the knockdown of circ_0007762 or miR-18a-5p and the intervention of TGF-β1 or 3-MA. Western blot assay was applied to determine the expression of a-SMA, collagen Ⅰ, P62 and LC3B Ⅱ/Ⅰ after the knockdown of circ_0007762 or miR-18a-5p and the intervention of TGF-β1 or 3-MA. Results　In contrast with the control group, the level of circ_0007762 in HFL1 was significantly up-regulated in the TGF-β1 group, and the level of miR-18a-5p was significantly down-regulated (P＜0.05). Overexpression of miR-18a-5p inhibited the luciferase activity in circ_0007762 wild-type vector (P＜0.05). The cell proliferation activity was decreased after knocking-down circ_0007762, while the effect could be rescued by the inhibition of miR-18a-5p. Meanwhile, 3-MA reversed TGF-β 1-induced fibroblast proliferation (P＜0.05). TGF-β1 promoted the levels of a-SMA, collagen Ⅰ and LC3B Ⅱ/Ⅰ, and inhibited the level of P62 (P＜0.05). Compared with the TGF-β1+si-NC group, a-SMA, collagen Ⅰ and LC3B Ⅱ/Ⅰ were down-regulated in the TGF-β1+si-circ_0007762 group, while P62 expression was increased, and the effect could be rescued by the suppression of miR-18a-5p (P＜0.05). Besides, 3-MA enhanced the expression of P62 and suppressed the expression levels of other proteins (P＜0.05). Conclusion　The circ_0007762 can interact with miR-18a-5p to accelerate the proliferation of lung fibroblasts and induce the fibrotic phenotype by activating autophagy.

Key words: idiopathic pulmonary fibrosis, autophagy, cell proliferation, fibroblasts, transforming growth factor beta, circ_0007762, miR-18a-5p