Targeting Galectin-3 to modulate inflammation in LAMA2-deficient congenital muscular dystrophy.

ABSTRACT: LAMA2-deficient congenital muscular dystrophy (LAMA2-CMD) is a severe neuromuscular disorder characterized by muscle degeneration, chronic inflammation, and fibrosis. While inflammation is one the hallmarks of LAMA2-CMD, the immune cell composition in laminin-deficient muscles remains understudied. Consequently, targeted pharmacological intervention to reduce inflammation remains underexplored. Here, we characterized the immune landscape in the dyW mouse model of LAMA2-CMD using RNA sequencing and flow cytometry. Transcriptomic analysis of dyW quadriceps femoris muscle identified 2,143 differentially expressed genes, with most upregulated genes linked to immune-related pathways. Lgals3 (Galectin-3) was significantly upregulated and identified as a key upstream regulator of the immun

SUBMITTER: de Menezes YKT 

PROVIDER: S-EPMC11952532 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature