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Previous research has suggested that autophagy and angiogenesis play vital roles in the prevention of heart failure after MI, and\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      is considered to be an important regulatory factor in MI. But the specific mechanism remains unknown. In this study, using cultured venous endothelial cells and a rat model of MI, we aimed to identify the potential target genes of\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      and discover the mechanisms of inhibiting autophagy and angiogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We first explored the biological functions of\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      on autophagy and angiogenesis on endothelial cells. Then we identified\n                      <jats:italic>ATG7<\/jats:italic>\n                      , which was the downstream target gene of\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      . The expression of\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      and\n                      <jats:italic>ATG7<\/jats:italic>\n                      was investigated in the rat model of MI.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found that miR\u2010106a inhibits the proliferation, cell cycle, autophagy and angiogenesis, but promoted the apoptosis of vein endothelial cells. Moreover,\n                      <jats:italic>ATG7<\/jats:italic>\n                      was identified as the target of\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      , and\n                      <jats:italic>ATG7<\/jats:italic>\n                      rescued the inhibition of autophagy and angiogenesis by\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      . The expression of miR\u2010106a in the rat model of MI was decreased but the expression of\n                      <jats:italic>ATG7<\/jats:italic>\n                      was increased in the infarction areas.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our results indicate that\n                      <jats:italic>miR\u2010106a<\/jats:italic>\n                      may inhibit autophagy and angiogenesis by targeting\n                      <jats:italic>ATG7<\/jats:italic>\n                      . This mechanism may be a potential therapeutic treatment for MI.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ame2.12418","type":"journal-article","created":{"date-parts":[[2024,5,29]],"date-time":"2024-05-29T00:45:46Z","timestamp":1716943546000},"page":"408-418","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["<i>MiR\u2010106a<\/i>\n                    targets\n                    <i>ATG7<\/i>\n                    to inhibit autophagy and angiogenesis after myocardial infarction"],"prefix":"10.1002","volume":"7","author":[{"given":"Guofeng","family":"Bai","sequence":"first","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Laboratory Animals Guangdong Laboratory Animals Monitoring Institute  Guangzhou China"},{"name":"Guangdong Laboratory of Lingnan Modern Agriculture, National Engineering Research Center for Breeding Swine Industry, State Key Laboratory of Swine and 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