This study aims to investigate the expression of the SLC25 subfamily in sepsis-associated acute kidney injury (SA-AKI) and the role ofin regulating PINK1/PARKIN-mediated mitophagy. Transcriptome sequencing of renal tissues from lipopolysaccharide (LPS)-induced SA-AKI rats at multiple time points revealed time-dependent differential expression of SLC25 genes. At 12 h post-LPS injection (renal injury peak), 11 differentially expressed genes were identified. Intersection with Gene Expression Omnibus datasets and Gene Ontology enrichment highlighted 11 codifferentially expressed genes enriched in mitochondrial transmembrane transport. Notably,was significantly negatively correlated with KIM-1 (= -0.96) and LCN2 (= -0.98).was significantly downregulated in SA-AKI rat renal tissues and LPS-induced HK-2 cells, accompanied by upregulated PINK1/PARKIN, excessive mitophagy (elevated LC3B-II, decreased p62), and increased renal injury markers.overexpression inhibited PINK1/PARKIN, reversed excessive mitophagy, reduced KIM-1 and LCN2 levels, alleviated mitochondrial dysfunction, enhanced cell viability, and exerted cytoprotective effects.knockdown attenuated the regulatory effect ofon excessive mitophagy, indicating a dependence on the PINK1/PARKIN pathway. In conclusion, downregulatedis closely associated with excessive mitophagy in SA-AKI.overexpression inhibits excessive mitophagy via downregulating the PINK1/PARKIN pathway, improves mitochondrial function, and alleviates HK-2 cell injury, suggesting thatmay be a novel molecular target for SA-AKI-targeted therapy. SLC25A30SLC25A30r r SLC25A30SLC25A30PINK1SLC25A30SLC25A30SLC25A30SLC25A30
