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• •The members and functions of IL-17 cytokine family are mentioned. • •IL-17 is involved in the occurrence of many inflammatory diseases, autoimmune diseases, and tumors. • •IL-17 is involved in acute renal injury caused by various reasons, such as sepsis associated acute renal injury, nephrotoxic acute renal injury, ischemia/reperfusion acute renal injury. Acute kidney injury (AKI) is a common clinical kidney disease with a high mortality rate. AKI is caused by a variety of factors, including sepsis, ischemia, and nephrotoxic drugs, and can progress to chronic kidney disease and end-stage renal disease. Numerous studies have suggested that cytokines can be used as therapeutic targets for AKI. IL-17 is a pro-inflammatory cytokine that not only participates in the host defense and the development of autoimmune diseases but also is linked to AKI due to a variety of factors. This review will give an overview of the structure, signaling pathways, and biological functions of IL-17, as well as its role in AKI, to show that IL-17 is a potential target for the prevention and treatment of AKI. [ABSTRACT FROM AUTHOR]

[Display omitted] Sepsis-associated acute kidney injury (SA-AKI) is a life-threatening condition associated with high mortality and morbidity. However, the underlying pathogenesis of SA-AKI is still unclear. Lyn belongs to Src family kinases (SFKs), which exert numerous biological functions including modulation in receptor-mediated intracellular signaling and intercellular communication. Previous studies demonstrated that Lyn gene deletion obviously aggravates LPS-induced lung inflammation, but the role and possible mechanism of Lyn in SA-AKI have not been reported yet. Here, we found that Lyn protected against renal tubular injury in cecal ligation and puncture (CLP) induced AKI mouse model by inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation and cell apoptosis. Moreover, Lyn agonist MLR-1023 pretreatment improved renal function, inhibited STAT3 phosphorylation and decreased cell apoptosis. Thus, Lyn appears to play a crucial role in orchestrating STAT3-mediated inflammation and cell apoptosis in SA-AKI. Hence, Lyn kinase may be a promising therapeutic target for SA-AKI. [ABSTRACT FROM AUTHOR]