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- W4309433281 abstract "Abstract Background To investigate the role of circNFIB in the alleviation of myocardial fibrosis by endogenous sulfur dioxide (SO 2 ). Methods We stimulated cultured neonatal rat cardiac fibroblasts with transforming growth factor-β1 (TGF-β1) and developed an in vitro myocardial fibrosis model. Lentivirus vectors containing aspartate aminotransferase 1 (AAT1) cDNA were used to overexpress AAT1, and siRNA was used to silence circNFIB. The SO 2 , collagen, circNFIB, Wnt/β-catenin, and p38 MAPK pathways were examined in each group. Results In the in vitro TGF-β1-induced myocardial fibrosis model, endogenous SO 2 /AAT1 expression was significantly decreased, and collagen levels in the cell supernatant and type I and III collagen expression, as well as α-SMA expression, were all significantly increased. TGF-β1 also significantly reduced circNFIB expression. AAT1 overexpression significantly reduced myocardial fibrosis while significantly increasing circNFIB expression. Endogenous SO 2 alleviated myocardial fibrosis after circNFIB expression was blocked. We discovered that circNFIB plays an important role in the alleviation of myocardial fibrosis by endogenous SO 2 by inhibiting the Wnt/β-catenin and p38 MAPK pathways. Conclusion Endogenous SO 2 promotes circNFIB expression, which inhibits the Wnt/β-catenin and p38 MAPK signaling pathways, consequently alleviating myocardial fibrosis." @default.
- W4309433281 created "2022-11-27" @default.
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- W4309433281 date "2022-11-20" @default.
- W4309433281 modified "2023-09-29" @default.
- W4309433281 title "Elucidating the role of circNFIB in myocardial fibrosis alleviation by endogenous sulfur dioxide" @default.
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- W4309433281 doi "https://doi.org/10.1186/s12872-022-02909-x" @default.
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