{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T05:43:04Z","timestamp":1777873384888,"version":"3.51.4"},"reference-count":59,"publisher":"Frontiers Media SA","issue":"5","license":[{"start":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T00:00:00Z","timestamp":1241136000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Exp Biol Med (Maywood)"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>\n                    Aims: Reactive oxygen species (ROS) activate multiple signaling pathways involved in cardiac hypertrophy. Since HO-1 exerts potent antioxidant effects, we hypothesized that this enzyme inhibits ROS-induced cardiomyocyte hypertrophy. Methods: HL-1 cardiomyocytes were transduced with an adenovirus constitutively expressing HO-1 (AdHO-1) to increase basal HO-1 expression and then exposed to 200 \u03bcM hydrogen peroxide (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ). Hypertrophy was measured using\n                    <jats:sup>3<\/jats:sup>\n                    H-leucine incorporation, planar morphometry and cell-size by forward-scatter flow-cytometry. The pro-oxidant effect of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    was assessed by redox sensitive fluorophores. Inducing intracellular redox imbalance resulted in cardiomyocyte hypertrophy through transactivation of nuclear factor kappa B (NF-\u03baB). Results: Pre-emptive HO-1 overexpression attenuated the redox imbalance and reduced hypertrophic indices. This is the first time that HO-1 has directly been shown to inhibit oxidant-induced cardiomyocyte hypertrophy by a NF-\u03baB\u2013dependent mechanism. Conclusion: These results demonstrate that HO-1 inhibits pro-oxidant induced cardiomyocyte hypertrophy and suggest that HO-1 may yield therapeutic potential in treatment of\n                  <\/jats:p>","DOI":"10.3181\/0810-rm-312","type":"journal-article","created":{"date-parts":[[2009,2,25]],"date-time":"2009-02-25T21:50:24Z","timestamp":1235598624000},"page":"582-594","source":"Crossref","is-referenced-by-count":33,"title":["Heme Oxygenase-1 Inhibits Pro-Oxidant Induced Hypertrophy in HL-1                Cardiomyocytes"],"prefix":"10.3389","volume":"234","author":[{"given":"Keith R.","family":"Brunt","sequence":"first","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew R.","family":"Tsuji","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joyce H.","family":"Lai","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert T.","family":"Kinobe","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William","family":"Durante","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William C.","family":"Claycomb","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher A.","family":"Ward","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luis G.","family":"Melo","sequence":"additional","affiliation":[{"name":"Department of Physiology, Queen\u2019s University, Kingston, Ontario, K7L\r               3N6 Canada; Department of Medical Pharmacology and Physiology, University of\r               Missouri, Columbia, Missouri 65212; and Department of Biochemistry and Molecular Biology, Louisiana State\r               University, Health Sciences Center, New Orleans, Louisiana 70112-1394"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2009,5,1]]},"reference":[{"key":"bibr-R1","unstructured":"Frey N, Olson EN. 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Role of TLR-2 in the\n               activation of nuclear factor kappaB by oxidative stress in cardiac myocytes.\n                  J Biol Chem 276(7):5197\u20135203, 2007.","DOI":"10.1074\/jbc.M009160200"},{"key":"bibr-R44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M103276200"},{"key":"bibr-R45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206175200"},{"key":"bibr-R46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M508416200"},{"key":"bibr-R47","doi-asserted-by":"publisher","DOI":"10.1126\/science.1130481"},{"key":"bibr-R48","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000254415.31362.a7"},{"key":"bibr-R49","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2006.8.1081"},{"key":"bibr-R50","unstructured":"Liu XL, Murduck J, Tsuji M, Tse Y, Pang SC, Melo LG.\n               Exogenous heme oxygenase-1 induction reduces cardiac hypertrophy in response to\n               aortic coarctation: Implications for treatment of heart failure. 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