Lupus nephritis (LN) is a highly complex autoimmune disease caused by systemic lupus erythematosus (SLE). MicroRNAs (miRNAs) play a vital role in the pathogenesis of SLE. Previously, a total of 29 miRNAs were identified to be down‐regulated in SLE patients, in which miR‐410 was likely to be involved in the signalling transduction pathways in regulating the pathogenesis of SLE. The purpose of this study was to investigate the role of miR‐410 in LN and to find out whether miR‐410 regulates the expression of interleukin (IL)‐6 and fibrosis in LN. It was found that the expression level of miR‐410 in kidney tissue of MRL/lpr mice was decreased compared to that in BALB/C mice, whereas the level of IL‐6 was overexpressed in MRL/lpr mice. Luciferase assay showed that miR‐410 binds directly to the 3′ untranslated region (UTR) of IL‐6, with the results showing that overexpression of miR‐410 significantly decreased the expression level of IL‐6 in SV40MES13 cells. Moreover, overexpression of miR‐410 significantly reduced the expression levels of fibrosis factors such as transforming growth factor‐β1 (TGF‐β1) and collagen I/III in SV40MES13 cells; Inhibition of the expression of miR‐410 with miR‐410 inhibitor resulted in increased levels of IL‐6 as well as fibrosis factors. The results identify that miR‐410, as a novel and critical factor in the pathogenesis of LN, decreases IL‐6 expression by binding directly to the 3′UTR and suppresses fibrosis through down‐regulation of TGF‐β1 in SV40MES13 cells. Our study brings new insight into understanding the complex mechanisms involved in the pathogenesis of lupus disease.