Small extracellular vesicles containing miR-486-5p promote angiogenesis after myocardial infarction in mice and nonhuman primates
Qingju Li, Qingju Li, Yinchuan Xu, Kaiqi Lv, Yingchao Wang, Zhiwei Zhong, Changchen Xiao, Keyang Zhu, Cheng Ni, Kan Wang, Minjian Kong, Xuebiao Li, Youqi Fan, Fengjiang Zhang, Qi Chen, Yi Li, Qian Li, Qian Li, Chengjia Liu, Jinyun Zhu, Shuhan Zhong, Jingyi Wang, Jingyi Wang, Yongjian Chen, Jing Zhao, Dan Zhu, Rongrong Wu, Jinghai Chen, Wei Zhu, Hong Yu, Reza Ardehali, Jianyi Zhang, Jianan Wang, Jianan Wang, Xinyang Hu
Abstract
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.