Delivery of miR-486-5p-engineered small extracellular vesicles safely enhanced angiogenesis and cardiac function in a nonhuman primate myocardial infarction model without increasing arrhythmias.
Does miR-486-5p-overexpressing N-sEV treatment improve angiogenesis and cardiac recovery in mice and nonhuman primate myocardial infarction models?
Delivery of miR-486-5p-engineered small extracellular vesicles safely enhanced angiogenesis and cardiac function in preclinical MI models, highlighting a potential strategy for cardiac repair.
silencing in CFs reduced the cleavage of extracellular vascular endothelial growth factor (VEGF). Furthermore, miR-486-5p-overexpressing N-sEV treatment promoted angiogenesis and cardiac recovery without increasing arrhythmia complications in a nonhuman primate (NHP) MI model. Collectively, this study highlights the key role of sEV miR-486-5p in promoting cardiac angiogenesis via fibroblastic MMP19-VEGFA cleavage signaling. Delivery of miR-486-5p-engineered sEVs safely enhanced angiogenesis and cardiac function in an NHP MI model and may promote cardiac repair.
Li et al. (Wed,) conducted a other in Myocardial infarction. miR-486-5p-overexpressing N-sEV treatment was evaluated on Angiogenesis and cardiac recovery. Delivery of miR-486-5p-engineered small extracellular vesicles safely enhanced angiogenesis and cardiac function in a nonhuman primate myocardial infarction model without increasing arrhythmias.