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However, the potential mechanism of M1 phenotype bone marrow\u2010derived macrophages\u2010 (BMMs\u2010) EVs (M1\u2010BMMs\u2010EVs) in MI is largely unknown. This study sought to investigate whether M1\u2010BMMs\u2010EVs increased CDC42 expression and activated the MEK\/ERK pathway by carrying lncRNA MALAT1 and competitively binding to miR\u201025\u20103p, thus inhibiting angiogenesis and myocardial regeneration after MI. After EV treatment, the cardiac function, infarct size, fibrosis, angiogenesis, and myocardial regeneration of MI mice and the viability, proliferation and angiogenesis of oxygen\u2010glucose deprivation\u2010 (OGD\u2010) treated myocardial microvascular endothelial cells (MMECs) were assessed. MALAT1 expression in MI mice, cells, and EVs was detected. MALAT1 downstream microRNAs (miRs), genes, and pathways were predicted and verified. MALAT1 and miR\u201025\u20103p were intervened to evaluate EV effects on OGD\u2010treated cells. In MI mice, EV treatment aggravated MI and inhibited angiogenesis and myocardial regeneration. In OGD\u2010treated cells, EV treatment suppressed cell viability, proliferation, and angiogenesis. MALAT1 was highly expressed in MI mice, OGD\u2010treated MMECs, M1\u2010BMMs, and EVs. Silencing MALAT1 weakened the inhibition of EV treatment on OGD\u2010treated cells. MALAT1 sponged miR\u201025\u20103p to upregulate CDC42. miR\u201025\u20103p overexpression promoted OGD\u2010treated cell viability, proliferation, and angiogenesis. The MEK\/ERK pathway was activated after EV treatment. Collectively, M1\u2010BMMs\u2010EVs inhibited angiogenesis and myocardial regeneration following MI via the MALAT1\/miR\u201025\u20103p\/CDC42 axis and the MEK\/ERK pathway activation.<\/jats:p>","DOI":"10.1155\/2021\/9959746","type":"journal-article","created":{"date-parts":[[2021,10,30]],"date-time":"2021-10-30T00:20:10Z","timestamp":1635553210000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["M1 Bone Marrow\u2010Derived Macrophage\u2010Derived Extracellular Vesicles Inhibit Angiogenesis and Myocardial Regeneration Following Myocardial Infarction via the MALAT1\/MicroRNA\u201025\u20103p\/CDC42 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