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treatment, miR-124-3p expression was reduced, while the mRNA and protein expression levels of HMGB1, TLR4, and NF-κB p65 were increased. A luciferase reporter assay confirmed the specific binding between miR-124-3p and HMGB1. Furthermore, overexpression of miR-124-3p significantly inhibited the HMGB1/TLR4/NF-κB signaling pathway and suppressed the expression of fibrotic factors. Collectively, our findings demonstrate that chronic arsenic exposure promotes renal fibrosis and renal injury by downregulating miR-124-3p expression, which in turn activates the HMGB1/TLR4/NF-κB signaling pathway.
Zhao et al. (Tue,) studied this question.