{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:32:50Z","timestamp":1791847970418,"version":"4.3.4"},"reference-count":70,"publisher":"SAGE Publications","issue":"14","license":[{"start":{"date-parts":[[2014,11,1]],"date-time":"2014-11-01T00:00:00Z","timestamp":1414800000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2014,11,1]],"date-time":"2014-11-01T00:00:00Z","timestamp":1414800000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2014,11]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aims:<\/jats:italic>\n                    <\/jats:bold>\n                    Small ubiquitin-like modifier type 1 (SUMO-1) has been shown to play a critical role in the dysfunction of the cardiac isoform of sarcoplasmic reticulum calcium ATPase (SERCA2a) pump in the setting of heart failure. In cardiac hypertrophy, the role of SUMO-1 has not been defined and our study's goals were to examine the effects of modulating SUMO-1 on the hypertrophic response both\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    and to examine whether oxidative stress (during cardiac hypertrophy) is abrogated by\n                    <jats:italic toggle=\"yes\">SUMO-1<\/jats:italic>\n                    gene transfer.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    In mice undergoing transverse aortic constriction (TAC), SUMO-1 levels increased slightly during the compensated stage of hypertrophy and then dropped sharply during the transition to heart failure. In isolated cardiomyocytes,\n                    <jats:italic toggle=\"yes\">SUMO-1<\/jats:italic>\n                    gene transfer inhibited the hypertrophic response in the presence of phenylephrine. Adeno-associated vector type 9 (AAV9) gene transfer of\n                    <jats:italic toggle=\"yes\">SUMO-1<\/jats:italic>\n                    prevented the heart from undergoing hypertrophy after TAC and prevented the development of left ventricular dysfunction. Furthermore,\n                    <jats:italic toggle=\"yes\">SUMO-1<\/jats:italic>\n                    gene transfer blocked the negative effects of H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    on SERCA2a activity in cardiac myocytes, while\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    indices of oxidative stress were decreased by SUMO-1 in cardiac hypertrophy and heart failure.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation and Conclusion:<\/jats:italic>\n                    <\/jats:bold>\n                    The results of this study indicate that post-translational modifications of SERCA2a caused by the toxic environment of the hypertrophied and failing myocardium can be prevented by SUMO-1.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    21, 1986\u20132001.\n                  <\/jats:p>","DOI":"10.1089\/ars.2014.5983","type":"journal-article","created":{"date-parts":[[2014,6,3]],"date-time":"2014-06-03T11:57:32Z","timestamp":1401796652000},"page":"1986-2001","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":62,"title":["The Role of SUMO-1 in Cardiac Oxidative Stress and Hypertrophy"],"prefix":"10.1177","volume":"21","author":[{"given":"Ahyoung","family":"Lee","sequence":"first","affiliation":[{"name":"Cardiovascular Research Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongtak","family":"Jeong","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinichi","family":"Mitsuyama","sequence":"additional","affiliation":[{"name":"Cardiovascular Research 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