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The role\u00a0of autophagy in the process of atherosclerosis has\u00a0drawn increasing attention. The human umbilical vein endothelial cells (HUVECs), whose Ras\u2010related C3 botulinum toxin substrate 1 (Rac1) and Rac3 was knockdown, were used to detect whether the possible molecular mechanisms of Rac1 and Rac3 for anti\u2010inflammatory in endothelial cells was effected by downregulation of autophagy. The HUVECs were incubated with ox\u2010LDL. The inflammatory factors and autophagy proteins were evaluated to ascertain and compare the effect of Rac1 and Rac3 on autophagy. Then, 3\u2010methyladenine (3\u2010MA) as an inhibiter of autophagy was used to detect whether the effect of Rac1 and Rac3 was related to autophagy. ox\u2010LDL\u2010induced cell dysfunction in HUVECs was determined by testing the formation of foam cells, the expression of nuclear factor (NF)\u2010\u03baB and nucleotide\u2010binding oligomerization domain (NOD)\u2010like receptor protein 3 and NF\u2010\u03baB p65 and other inflammatory factors, the release of reactive oxygen species by oxidative stress and the dysfunction of the cytomembrane. And ApoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice on a high\u2010fat diet were used as an animal model to detect the effect of Rac1 and Rac3 in vivo. The results showed that when Rac1 and Rac3 were decreased in HUVECs, the cell dysfunction caused by ox\u2010LDL was inhibited. If 3\u2010MA was used to inhibit autophagy in Rac1 and Rac3\u00a0knockdown cells, the injury induced by ox\u2010LDL on the cells was recovered. These results indicated that the effect of Rac1 and Rac3 was combined with ox\u2010LDL, which was related to inhibition\u00a0of autophagy. The effect of\u00a0Rac3 was more significant than that of Rac1.<\/jats:p>","DOI":"10.1002\/jcp.29072","type":"journal-article","created":{"date-parts":[[2019,7,23]],"date-time":"2019-07-23T00:07:25Z","timestamp":1563840445000},"page":"1531-1542","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Rac3, but not Rac1, promotes ox\u2010LDL induced endothelial dysfunction by downregulating autophagy"],"prefix":"10.1002","volume":"235","author":[{"given":"Dan","family":"He","sequence":"first","affiliation":[{"name":"Institute of Heart and Vessel Diseases The Second Affiliated Hospital of Dalian Medical University, Dalian Medical University  Dalian China"},{"name":"Department of Cardiology The Second Affiliated Hospital of Dalian Medical University  Dalian China"},{"name":"Key Laboratory of Myocardial Ischemia, Ministry of Education Harbin Medical University  Harbin 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