4.7 Article

Fluvoxamine alleviates bleomycin-induced lung fibrosis via regulating the cGAS-STING pathway

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PHARMACOLOGICAL RESEARCH
卷 187, 期 -, 页码 -

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ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2022.106577

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Idiopathic pulmonary fibrosis (IPF); Cyclic GMP-AMP synthase (cGAS); Stimulator of interferon genes (STING); Fluvoxamine; Bleomycin

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Fluvoxamine exhibits therapeutic activities in IPF by inhibiting fibroblast activation and migration, reducing inflammation and excessive extracellular matrix production, and improving pulmonary function.
Idiopathic pulmonary fibrosis (IPF) is a fatal disease with high mortality and limited effective therapy. Herein, we reported that fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), used in depression and anxiety treatment, also exhibited therapeutic activities in IPF. Fluvoxamine inhibited cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING), restrained the activation of their downstream targets, including PERK/ eIF2 alpha/ c-Myc/ miR-9-5p/ TBPL1 and TBK1/ YAP/ JNK1/2/ Bnip3/ CaMKII/ cofilin signaling, thus attenuated the activation and migration of fibroblasts upon TGF-beta 1 challenge. Fluvoxamine dose-dependently improved pulmonary function, decreased the expression of inflammatory factors, reduced excessive produc-tion of extracellular matrix, and thus alleviated bleomycin (BLM)-induced lung fibrosis in mice. Moreover, flu-voxamine at a dose of 10 mg/ kg showed similar efficacy as pirfenidone (PFD) at a dose of 30 mg/kg in a mice model of lung fibrosis. In summary, our results suggest that fluvoxamine is an effective anti-fibrotic agent for IPF.

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