{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T14:12:32Z","timestamp":1793196752512,"version":"4.5.0"},"reference-count":59,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2018,3,2]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>An elevated level of plasma LDL (low-density lipoprotein) is an established risk factor for cardiovascular disease. Recently, we reported that the (pro)renin receptor ([P]RR) regulates LDL metabolism in vitro via the LDLR (LDL receptor) and SORT1 (sortilin-1), independently of the renin\u2013angiotensin system.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objectives:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>To investigate the physiological role of (P)RR in lipid metabolism in vivo.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>We used N-acetylgalactosamine modified antisense oligonucleotides to specifically inhibit hepatic (P)RR expression in C57BL\/6 mice and studied the consequences this has on lipid metabolism. In line with our earlier report, hepatic (P)RR silencing increased plasma LDL-C (LDL cholesterol). Unexpectedly, this also resulted in markedly reduced plasma triglycerides in a SORT1-independent manner in C57BL\/6 mice fed a normal- or high-fat diet. In LDLR-deficient mice, hepatic (P)RR inhibition reduced both plasma cholesterol and triglycerides, in a diet-independent manner. Mechanistically, we found that (P)RR inhibition decreased protein abundance of ACC (acetyl-CoA carboxylase) and PDH (pyruvate dehydrogenase). This alteration reprograms hepatic metabolism, leading to reduced lipid synthesis and increased fatty acid oxidation. As a result, hepatic (P)RR inhibition attenuated diet-induced obesity and hepatosteatosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Collectively, our study suggests that (P)RR plays a key role in energy homeostasis and regulation of plasma lipids by integrating hepatic glucose and lipid metabolism.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.117.312422","type":"journal-article","created":{"date-parts":[[2018,1,4]],"date-time":"2018-01-04T10:15:44Z","timestamp":1515060944000},"page":"730-741","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":57,"title":["(Pro)renin Receptor Inhibition Reprograms Hepatic Lipid Metabolism and Protects Mice From Diet-Induced Obesity and Hepatosteatosis"],"prefix":"10.1161","volume":"122","author":[{"given":"Liwei","family":"Ren","sequence":"first","affiliation":[{"name":"From the AstraZeneca-Shenzhen University Joint Institute of Nephrology, Department of Physiology, Shenzhen University Health Science Center, Shenzhen University, China (L.R., Y.S., D.Y., L.H., N.W., M.W., F.S., W.T., J.S., X.R., X.L.); Translational Medicine Collaborative Innovation Center, The Second Clinical Medical College (Shenzhen People\u2019s Hospital) of Jinan University, Shenzhen, China (L.R., Y.S., F.L., X.L.); Division of Pharmacology and Vascular Medicine, Department of Internal Medicine,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Sun","sequence":"additional","affiliation":[{"name":"From the AstraZeneca-Shenzhen University Joint Institute of Nephrology, Department of Physiology, Shenzhen University Health Science Center, Shenzhen University, China (L.R., Y.S., D.Y., L.H., N.W., M.W., F.S., W.T., J.S., X.R., X.L.); Translational Medicine Collaborative Innovation Center, The Second Clinical Medical College (Shenzhen People\u2019s Hospital) of Jinan University, Shenzhen, China (L.R., Y.S., F.L., X.L.); Division of Pharmacology and Vascular Medicine, Department of Internal Medicine,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Lu","sequence":"additional","affiliation":[{"name":"From the AstraZeneca-Shenzhen University Joint Institute of Nephrology, Department of Physiology, Shenzhen University Health Science Center, Shenzhen University, China (L.R., Y.S., D.Y., L.H., N.W., M.W., F.S., W.T., J.S., X.R., X.L.); Translational Medicine Collaborative Innovation Center, The Second Clinical Medical College (Shenzhen People\u2019s Hospital) of Jinan University, Shenzhen, China (L.R., Y.S., F.L., X.L.); Division of Pharmacology and Vascular Medicine, Department of Internal Medicine,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dien","family":"Ye","sequence":"additional","affiliation":[{"name":"From the AstraZeneca-Shenzhen University Joint Institute of Nephrology, Department of Physiology, Shenzhen University Health Science Center, Shenzhen University, China (L.R., Y.S., D.Y., L.H., N.W., M.W., F.S., W.T., J.S., X.R., X.L.); Translational Medicine Collaborative Innovation Center, The Second Clinical Medical College (Shenzhen People\u2019s Hospital) of Jinan University, Shenzhen, China (L.R., Y.S., F.L., X.L.); Division of Pharmacology and Vascular Medicine, Department of Internal Medicine,..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lijuan","family":"Han","sequence":"additional","affiliation":[{"name":"From the AstraZeneca-Shenzhen University Joint Institute of Nephrology, Department of Physiology, Shenzhen University Health Science Center, Shenzhen University, China (L.R., Y.S., D.Y., L.H., N.W., M.W., F.S., W.T., J.S., X.R., X.L.); 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