Renal fibrosis is the common and final histopathological feature for many kidney diseases.IL-17A has recently been shown to be a proinflammatory cytokine involved in chronic inflammation and autoimmune disease.Our former study found that IL-17A participates in the development and progression of pulmonary fibrosis.In our recent study, we found IL-17A expression to be elevated and IL-17A-associated signaling pathways to be activated in the renal fibrosis model of unilateral ureteral occlusion (UUO) C3H/He mice.Neutralization of IL-17A in vivo attenuated renal fibrosis, and increased survival.Moreover, both in vitro and in the UUO mice, we found the expression of senescence-associated secretory phenotypes (SASPs) to be elvated and senescence signaling pathways to be activated.Our results indicated that the components of the IL-17A signaling pathways are potential therapeutic targets for the treatment of fibroproliferative kidney diseases and cellular senescence may be involved in the development and progression of renal fibrosis.