In a mouse MI model, a ROS-responsive hydrogel delivering miR-21 and DB1976 significantly improved cardiac function by remodeling multiple cell types in the cardiac microenvironment.
Does a ROS-responsive hydrogel delivering miR-21 and DB1976 improve cardiac function and tissue remodeling in a mouse MI model?
A novel ROS-responsive hydrogel delivering miR-21 and a PU.1 inhibitor significantly improved cardiac function and tissue remodeling in a mouse model of myocardial infarction.
ABSTRACT Myocardial infarction (MI) is a worldwide disease with high prevalence and mortality, but it still lacks efficient therapeutic strategies. Since it has been found that numerous cell types are involved in the pathological changes of MI, including fibroblasts, cardiomyocytes, immune cells, and endothelial cells, targeting a cell type seems no longer the ideal treatment. Here, we developed a ROS‐responsive delivery system for microRNA‐21 (miR‐21) and DB1976 (a PU.1 inhibitor) to remodel the cardiac environment in a relatively comprehensive way. MiR‐21 exhibited cardioprotective effects by improving angiogenesis, reducing apoptosis, and combating inflammation. However, the accompanying fibrosis impedes its therapeutic effect. DB1976, as a PU.1 inhibitor, could effectively inhibit fibrosis and alleviate the adverse effects of miR‐21. In a mouse MI model, the hydrogel (termed mesoporous silica nanoparticles (MSN)/miR‐21‐DB hydrogel) significantly improved cardiac function through remodeling cardiomyocytes, macrophages, fibroblasts, and vascular endothelial cells. This work provides a new approach for repairing damaged cardiac tissue by simultaneously regulating multiple cell types in the cardiac microenvironment.
Feng et al. (Sat,) conducted a other in Myocardial infarction. MSN/miR-21-DB hydrogel (ROS-responsive delivery system for miR-21 and DB1976) was evaluated on Cardiac function and remodeling of cardiomyocytes, macrophages, fibroblasts, and vascular endothelial cells. In a mouse MI model, a ROS-responsive hydrogel delivering miR-21 and DB1976 significantly improved cardiac function by remodeling multiple cell types in the cardiac microenvironment.