- In Duchenne muscular dystrophy (DMD), macrophages release chondroitin sulfate proteoglycan-4 (CSPG4), contributing to heart dysfunction.
- CSPG4 disrupts the neuro-cardiac junction, exacerbating heart function loss.
- Givinostat, a histone deacetylase inhibitor, reduced CSPG4 levels and restored normal neuro-cardiac signaling in mouse models.
- Potential therapy targets were identified for conditions involving cardiac fibrosis and inflammation.
- Questions remain regarding the translation of findings to human patients and the timing of intervention for therapeutic benefit.
How Immune Cells Sabotage the Heart in Duchenne Muscular Dystrophy
Conexiant
November 12, 2024