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HDL\u2010targeted therapeutic strategy for atherosclerotic cardiovascular disease (CVD) is currently under development. This study aims to assess the role of methionine sulfoxide reductase A (MsrA) in abnormal HDL and its related disorders in scavenger receptor class B type I deficient (\n                    <jats:italic>\n                      SR\u2010BI\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ) mice.\u00a0First, we demonstrated that MsrA overexpression attenuated ROS level and inflammation in HepG2 cells. For the in vivo study,\n                    <jats:italic>\n                      SR\u2010BI\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice were intravenously injected with lentivirus to achieve hepatic MsrA overexpression. High\u2010level hepatic MsrA significantly reduced the plasma free cholesterol contents, improved HDL functional proteins apolipoprotein A\u2010I (apoAI), apoE, paraoxonase1 (PON1), and lecithin:cholesterol acyltransferase (LCAT), while decreased the pro\u2010inflammatory property of dysfunctional HDL, contributing to reduced atherosclerosis and hepatic steatosis in Western diet\u2010fed mice. Furthermore, the study revealed that hepatic MsrA altered the expression of several genes controlling HDL biogenesis, cholesterol esterification, cholesterol uptake mediated by low\u2010density lipoprotein receptor (LDLR) and biliary excretion, as well as suppressed nuclear factor \u03baB (NF\u2010\u03baB) signaling pathway, which largely relied on liver X receptor alpha (LXR\u03b1)\u2010upregulation. These results provide original evidence that MsrA may be a promising target for the therapy of dysfunctional HDL\u2010related CVD.\n                  <\/jats:p>","DOI":"10.1096\/fj.201902429r","type":"journal-article","created":{"date-parts":[[2020,1,24]],"date-time":"2020-01-24T01:40:55Z","timestamp":1579830055000},"page":"3805-3819","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Methionine sulfoxide reductase A attenuates atherosclerosis via repairing dysfunctional HDL in scavenger receptor class B type I deficient mice"],"prefix":"10.1096","volume":"34","author":[{"given":"Yanyong","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Hubei Provincial Key Laboratory of Developmentally Originated Disease Wuhan University School of Basic Medical Sciences Wuhan 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China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Binyi","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Hubei Provincial Key Laboratory of Developmentally Originated Disease Wuhan University School of Basic Medical Sciences Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yiyong","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Hubei Provincial Key Laboratory of Developmentally Originated Disease Wuhan University School of Basic Medical Sciences Wuhan China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jia","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Hubei Provincial Key Laboratory of Developmentally Originated Disease Wuhan University School of Basic Medical Sciences Wuhan 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