{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T07:10:11Z","timestamp":1780643411874,"version":"3.54.1"},"reference-count":38,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T00:00:00Z","timestamp":1251763200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cardiovasc Pharmacol Ther"],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:p>\n                    3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as statins, have been shown to reduce cardiac remodeling. Angiotensin II (Ang II) type 1 receptor (AT1R) and oxidized low-density lipoprotein (ox-LDL) via its lectin-like ox-LDL receptor (LOX-1) are major stimuli for cardiomyocyte growth. We postulated that rosuvastatin, a potent HMG-CoA reductase inhibitor, may reduce Ang II\u2014mediated cardiomyocyte growth via AT1R and LOX-1 inhibition. HL-1 adult mouse cardiomyocytes were incubated overnight in serum-free medium, and then treated with rosuvastatin, the AT1R inhibitor losartan or anti-LOX-1 antibody for 3 hours. The cells were then stimulated with Ang II. We measured cardiomyocyte growth, and associated intracellular redox signals using reverse transcription\u2014 polymerase chain reaction (RT-PCR) and real-time quantitative PCR. Losartan and anti-LOX-1 antibody markedly attenuated Ang II\u2014mediated oxidant stress, and the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (p40\n                    <jats:sup>pho x<\/jats:sup>\n                    and gp91\n                    <jats:sup>phox<\/jats:sup>\n                    subunits) and nuclear factor-\u03baB (NF-\u03baB). Rosuvastatin attenuated the Ang II\u2014mediated upregulation of both subunits of NAPDH oxidase as well as NF-\u03baB. Rosuvastatin also reduced Ang II\u2014mediated upregulation of AT1R and LOX-1. In other experiments, LOX-1 was upregulated in cardiomyocytes by transfection with pCI-neo\/LOX-1, which also enhanced the expression AT1R messenger RNA (mRNA), and rosuvastatin pretreatment reduced the expression of both LOX-1 and AT1R in this system. Thus, rosuvastatin attenuates Ang II\u2014mediated cardiomyocyte growth by inhibiting LOX-1 and AT1R expression and suppressing the heightened intracellular redox state.\n                  <\/jats:p>","DOI":"10.1177\/1074248409344329","type":"journal-article","created":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T22:53:46Z","timestamp":1251845626000},"page":"283-291","source":"Crossref","is-referenced-by-count":29,"title":["Rosuvastatin Attenuates Ang II\u2014Mediated Cardiomyocyte Hypertrophy via Inhibition of LOX-1"],"prefix":"10.1177","volume":"14","author":[{"given":"Bum-Yong","family":"Kang","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jawahar L.","family":"Mehta","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Arkansas 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