"Chronic inflammation is a central driver of pathological fibrosis after ischaemic or haemodynamic stress, but strategies that locally rebalance injurious and reparative immune responses without systemic immunosuppression are lacking."
"Here we show that engineered immunosuppressive and fibrosis-targeted dendritic cells (iCDCs) effectively protect against pathological cardiac remodelling."
"In mouse models of ischaemia-reperfusion injury, myocardial infarction and pressure overload, iCDC therapy reduced inflammatory cardiac fibrosis, improved cardiac perfusion and preserved contractility."
"Mechanistically, iCDCs conferred sustained cardioprotection directly by suppressing immune and stromal cell activation or indirectly through other pathways."
Heart failure is a major health issue with no effective therapies for preventing or reversing cardiac fibrosis. Chronic inflammation drives this fibrosis, necessitating strategies that target immune responses without systemic immunosuppression. Engineered immunosuppressive dendritic cells (iCDCs) have been developed to address this issue. In mouse models, iCDC therapy significantly reduced inflammatory cardiac fibrosis, enhanced cardiac perfusion, and preserved heart contractility, demonstrating their potential for cardioprotection by modulating immune and stromal cell activity.
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