Galectin-3/CD146 interaction promotes renal damage and systemic inflammation after acute kidney injury.

ABSTRACT: Galectin-3 (Gal-3) expression is abnormally increased after renal ischemic injury, in various studies, further promoting tissue damage. Gal-3 may interact with the endothelial layer to induce inflammation during renal injury, linking the systemic and tissue compartments. However, this mechanism has not been investigated after acute kidney injury (AKI). To this end, wild-type (WT) and Gal-3-/- mice underwent renal ischemia followed by reperfusion (rIR). Bone marrow transplantation was used to differentiate Gal-3 expression in renal tissue from systemic bone marrow cells. WT mice were injected with recombinant Gal-3 to study systemic issues. Gal-3 expression was assessed by immunofluorescence, western blot, and scRNAseq. Systemic pathways were analyzed with plasma proteomics. Immunofluoresce

SUBMITTER: Boutin L 

PROVIDER: S-EPMC12644692 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature