Key result
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.
Why the study?
Does miR-486-5p-overexpressing N-sEV treatment improve angiogenesis and cardiac recovery in mice and nonhuman primate myocardial infarction models?
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.
No takes yet. Share an insight, caveat, or question.
Li et al. (2021) studied 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.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: