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Vascular endothelial growth factor (VEGF)\u2010A is a strong and essential proangiogenic factor. Reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and autophagy are implicated in the process of angiogenesis. This study is designed to clarify the regulatory mechanisms underlying VEGF\u2010A, ROS, ER stress, autophagy, and angiogenesis in acute myocardial infarction (AMI). A mouse model of AMI was successfully established by occluding the left anterior descending coronary artery. Compared with the sham\u2010operated mice, the microvessel density, VEGF\u2010A content, ROS production, expression of vascular endothelial cadherin, positive expression of 78\u2009kDa glucose\u2010regulated protein\/binding immunoglobulin protein (GRP78\/Bip), and LC3 puncta in CD31\u2010positive endothelial cells of the ischemic myocardium were overtly elevated. Moreover, VEGF\u2010A exposure predominantly increased the expression of beclin\u20101, autophagy\u2010related gene (ATG) 4, ATG5, inositol\u2010requiring enzyme\u20101 (IRE\u20101), GRP78\/Bip, and LC3\u2010II\/LC3\u2010I as well as ROS production in the human umbilical vein endothelial cells (HUVECs) in a dose and time\u2010dependent manner. Both beclin\u20101 small interfering RNA and 3\u2010methyladenine treatment predominantly mitigated VEGF\u2010A\u2010induced tube formation and migration of HUVECs, but they failed to elicit any notable effect on VEGF\u2010A\u2010increased expression of GRP78\/Bip. Tauroursodeoxycholic acid not only obviously abolished VEGF\u2010A\u2010induced increase of IRE\u20101, GRP78\/Bip, beclin\u20101 expression, and LC3\u2010II\/LC3\u2010I, but also negated VEGF\u2010A\u2010induced tube formation and migration of HUVECs. Furthermore,\n                    <jats:italic>N<\/jats:italic>\n                    \u2010acetyl\u2010\n                    <jats:sc>l<\/jats:sc>\n                    \u2010cysteine markedly abrogated VEGF\u2010A\u2010increased ROS production, IRE\u20101, GRP78\/Bip, beclin\u20101 expression, and LC3\u2010II\/LC3\u2010I in the HUVECs. Taken together, our data demonstrated that increased spontaneous production of VEGF\u2010A may induce angiogenesis after AMI through initiating ROS\u2013ER stress\u2010autophagy axis in the vascular endothelial cells.\n                  <\/jats:p>","DOI":"10.1002\/jcp.28395","type":"journal-article","created":{"date-parts":[[2019,2,22]],"date-time":"2019-02-22T00:06:28Z","timestamp":1550793988000},"page":"17690-17703","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":158,"title":["VEGF\u2010A promotes angiogenesis after acute myocardial infarction through increasing ROS production and enhancing ER stress\u2010mediated autophagy"],"prefix":"10.1002","volume":"234","author":[{"given":"Jiang","family":"Zou","sequence":"first","affiliation":[{"name":"Department of Pathophysiology School of Basic Medical Science, Central South University Changsha Hunan China"},{"name":"Key Laboratory of Sepsis Translational Medicine of Hunan, Central 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