CX3CL1 deficiency ameliorates acute kidney injury by inhibiting macrophage mitochondrial dysfunction and mtDNA-cGAS-STING signaling.

ABSTRACT: Dysregulated mitochondrial dynamics and macrophage-driven inflammation are essential contributors to the pathogenesis of acute kidney injury (AKI). Although the chemokine CX3CL1 has been associated with inflammatory responses, its role in AKI, particularly in regulating macrophage polarization and mitochondrial function, remains unclear. In this study, we investigated the therapeutic potential of CX3CL1 inhibition in a lipopolysaccharide (LPS)-induced AKI model. Our results found that CX3CL1 deficiency could significantly ameliorate renal dysfunction and attenuate inflammatory responses. RNA sequencing revealed that CX3CL1 deficiency alters macrophage subpopulations and gene expression profiles in the kidney, particularly affecting pathways related to immune responses and mitochondrial fun

SUBMITTER: Gong Q 

PROVIDER: S-EPMC12847948 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature