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Sepsis-associated acute kidney injury (SA-AKI) is a severe and life-threatening condition with high morbidity and mortality among emergency patients, and it poses a significant risk of chronic renal failure. Clinical treatments for SA-AKI remain reactive and non-specific, lacking effective diagnostic biomarkers or treatment targets. In this study, we established an SA-AKI mouse model using lipopolysaccharide (LPS) and performed proteomics and metabolomics analyses. A variety of bioinformatic analyses, including gene set enrichment analysis (GSEA), weighted gene co-expression network analysis (WGCNA), protein and protein interactions (PPI), and MetaboAnalyst analysis, were conducted to investigate the key molecules of SA-AKI. Integrated proteomics and metabolomics analysis revealed that sepsis led to impaired renal mitochondrial function and metabolic disorders. Immune-related pathways were found to be activated in kidneys upon septic infection. The catabolic products of polyamines accumulated in septic kidneys. Overall, our integrated analysis provides a multidimensional understanding of SA-AKI and identifies potential pathways for this condition. [ABSTRACT FROM AUTHOR]

Sepsis-associated acute renal injury (SA-AKI) is a common critical clinical disease. It is associated with increased mortality and increased risk of progression to chronic kidney disease. However, its pathogenesis is not fully known. We hypothesized that metabolic interactions mediate cell apoptosis and AKI. We found that phosphatidylcholine content in human renal tubular epithelial cells following lipopolysaccharide-induced injury was increased. The activity of lysophosphatidylcholine acyltransferase 3 (LPCAT3), a key enzyme in phospholipid metabolism, was increased, while the expression of miR-124-3p.1, which targets LPCAT3, was decreased. We also found that in the serum of SA-AKI patients, LPCAT3 activity was increased, and miR-124-3p.1 expression was decreased. Further experiments confirmed the specific binding of exocrine miR-124-3p.1 to LPCAT3. Our data reveal the molecular mechanisms of phospholipid metabolic disorder in early SA-AKI as well as the role of the miR-124-3p.1/LPCAT3 pathway in SA-AKI, which leads to ferroptosis. These results could provide the scientific basis for early diagnosis and renal replacement therapy in SA-AKI. • In early SA-AKI, the phospholipid metabolic disordered. • MiR-124-3p.1 can regulate LPCAT3 expression and affect lipid metabolism, which leads to ferroptosis. • These results could provide the scientific basis for early diagnosis and renal replacement therapy in SA-AKI. [ABSTRACT FROM AUTHOR]

• •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]