{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:19:20Z","timestamp":1784557160107,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"6","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:p>\n                    This study was conducted to test whether oxidative stress activates the intracellular protein kinase B (AKT1) signaling pathway, which culminates with cardiac hypertrophy in experimental hyperthyroidism. Male Wistar rats were divided into four groups: control, vitamin E, thyroxine (T\n                    <jats:sub>4<\/jats:sub>\n                    ), and T\n                    <jats:sub>4<\/jats:sub>\n                    +vitamin E. Hyperthyroidism was induced by T\n                    <jats:sub>4<\/jats:sub>\n                    administration (12\u200amg\/l in drinking water for 28 days). Vitamin E treatment was given during the same period via s.c. injections (20\u200amg\/kg per day). Morphometric and hemodynamic parameters were evaluated at the end of the 4-week treatment period. Protein oxidation, redox state (reduced glutathione, GSH\/glutathione dissulfide, GSSG), vitamin C, total radical-trapping antioxidant potential (TRAP), hydrogen peroxide (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ), and nitric oxide metabolites (NO\n                    <jats:sub>X<\/jats:sub>\n                    ) were measured in heart homogenates. The p-AKT1\/AKT1 ratio, p-glycogen-synthase kinase (GSK)3B\/GSK3B ratio, FOS, and JUN myocardial protein expression were also quantified by western blot after 4 weeks. Increases in biochemical parameters, such as protein oxidation (41%), H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    (62%), and NO\n                    <jats:sub>X<\/jats:sub>\n                    (218%), and increase in the left ventricular end-diastolic pressure were observed in the T\n                    <jats:sub>4<\/jats:sub>\n                    group. T\n                    <jats:sub>4<\/jats:sub>\n                    treatment also caused a decrease in GSH\/GSSG ratio (83%), vitamin C (34%), and TRAP (55%). These alterations were attenuated by vitamin E administration to the hyperthyroid rats. Expression of p-AKT1\/AKT1, p-GSK3B\/GSK3B, FOS, and JUN were elevated in the T\n                    <jats:sub>4<\/jats:sub>\n                    group (by 69, 37, 130, and 33% respectively), whereas vitamin E administration promoted a significant reduction in their expression. These results indicate that oxidative stress plays an important role in cardiac hypertrophy, and suggest redox activation of AKT1 and JUN\/FOS signaling pathways with H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    acting as a possible intracellular mediator in this adaptive response to experimental hyperthyroidism.\n                  <\/jats:p>","DOI":"10.1677\/jme-08-0024","type":"journal-article","created":{"date-parts":[[2008,9,11]],"date-time":"2008-09-11T20:45:33Z","timestamp":1221165933000},"page":"423-430","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":39,"title":["The role of redox signaling in cardiac hypertrophy induced by experimental hyperthyroidism"],"prefix":"10.1530","volume":"41","author":[{"given":"A S R","family":"Araujo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Schenkel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A T","family":"Enzveiler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T R G","family":"Fernandes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W A","family":"Partata","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Llesuy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M F M","family":"Ribeiro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N","family":"Khaper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P K","family":"Singal","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Bell\u00f3-Klein","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Molecular Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/jme.bioscientifica.com\/view\/journals\/jme\/41\/6\/423.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/jme.bioscientifica.com\/downloadpdf\/journals\/jme\/41\/6\/423.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:51:58Z","timestamp":1784555518000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/jme\/article\/41\/6\/423-430\/12010"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2008,9,11]]},"references-count":0,"journal-issue":{"issue":"6"},"URL":"https:\/\/doi.org\/10.1677\/jme-08-0024","relation":{},"ISSN":["0952-5041","1479-6813"],"issn-type":[{"value":"0952-5041","type":"print"},{"value":"1479-6813","type":"electronic"}],"subject":[],"published":{"date-parts":[[2008,9,11]]}}}