Lgals3 Promotes Calcium Oxalate Crystal Formation and Kidney Injury Through Histone Lactylation-Mediated FGFR4 Activation.

ABSTRACT: The incidence of kidney stones is increasing worldwide. However, the underlying mechanism of the process of kidney stone formation and the kidney damage caused are not well understood. Here, it is observed that Lgals3, a β-galactoside-binding protein, is significantly increased in tissues with calcium oxalate (CaOx) stones, and in both in vivo and in vitro models. Lgals3 expression is positively correlated with the deposition of CaOx crystals. Knockout of Lgals3 markedly reduces the deposition of CaOx crystal and renal fibrosis in vivo. Furthermore, Lgals3 deficiency decrease the glycolytic rate and lactate production during the process of CaOx deposition and inhibited histone lactylation of H3K18la. Mechanistic studies shows that Lgals3 directly interacted with the key glycolysis protein

SUBMITTER: Ye Z 

PROVIDER: S-EPMC11947994 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature