Endothelial cell senescence is closely related to the occurrence of cardiovascular diseases and microRNAs (miRNAs/miRs) are considered as therapeutic targets for cardiovascular disease. The current study aimed to investigate the role of miR-20b in the senescence process of endothelial cells and its underlying mechanism. cell viability, proportion of senescent cells and the cell cycle were respectively determined by cell counting Kit-8, SA-β-galactosidase and flow cytometry. The relative expressions of mRNA and protein were detected by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The possible target genes and binding sites of miR-20b were predicted using Targetscan and further verified by dual luciferase reporter assay. The present study found that H 2 O 2 inhibited cell viability, caused cell cycle arrest in G1 phase, decreased miR-20b level and induced cell senescence. Moreover, high expression of miR-20b promoted cell viability and reduced H 2 O 2-induced cell senescence, whereas low expression of miR-20b produced the opposite effects. Thioredoxin interacting protein (TXNIP) was predicted as a target gene for miR-20b and knockdown of TXNIP increased cell viability, inhibited cell senescence, reduced the expression of p16, p21, TXNIP, NLR family pyrin domain containing 3 (NLRP3) and cleaved caspase-1 and reversed the promoting effects of the miR-20b inhibitor and H 2 O 2 on cell senescence. Furthermore, the knockdown of TXNIP inhibited the Wnt/β-catenin pathway. The finding reveals that high expression of miR-20b inhibits the senescence of human umbilical vein endothelial cells through regulating the Wnt/β-catenin pathway via the TXNIP/NLRP3 axis.

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