Since excessive ECM deposition drives myocardial stiffness and dysfunction in DMD hearts, CSPG4.CAR-T treatment was found to markedly reduce the fibrotic area based on histology and downregulate key profibrotic genes (Tgf-β1, Fn1, Col1a1, Col3a1), indicating effective ECM remodeling. Here, COL3A1 is linked to Duchenne muscular dystrophy.