lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis
Yanni Yang(Kunming Medical University), Wenlin Tai(Kunming Medical University), Nihong Lu(Kunming Third People's Hospital), Ting Li(Kunming Medical University), Yongjun Liu(Kunming Medical University), Wenjuan Wu(Kunming Medical University), Zhengkun Li(Kunming Medical University), Lin Pu(Kunming Medical University), Xiaoyuan Zhao(Kunming Medical University), Tao Zhang(Kunming Medical University), Zhaoxing Dong(Kunming Medical University)
Cited by 177Open Access
Abstract
experiments showed that inhibition of lncRNA ZFAS1 abolished BLM-induced lipid peroxidation and PF development. Mechanistically, silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression. Collectively, our studies demonstrated the role of the lncRNA ZFAS1/miR-150-5p/SLC38A1 axis in the progression of PF, and may provide a new biomarker for the treatment of PF patients.
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