{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T22:04:24Z","timestamp":1791929064568,"version":"4.3.4"},"reference-count":64,"publisher":"SAGE Publications","issue":"9","license":[{"start":{"date-parts":[[2013,3,1]],"date-time":"2013-03-01T00:00:00Z","timestamp":1362096000000},"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":[[2013,3]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Significance:<\/jats:italic>\n                    <\/jats:bold>\n                    Many cardiovascular disorders are accompanied by a deregulated cellular redox balance resulting in elevated levels of intracellular reactive oxygen species (ROS). One major antioxidative cellular molecule is thioredoxin-1 (Trx-1). Its indispensability is demonstrated by the embryonic lethality of Trx-1 deficient mice. Trx-1 is ubiquitously expressed in cells and has numerous, diverse functions. It not only reduces oxidized proteins or, together with peroxiredoxins, detoxifies H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    , but also binds to several proteins and thereby regulates their functions. The interaction partners of Trx-1 differ depending on its localization in the cytosol or in the nucleus.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Recent Advances\/Critical Issues:<\/jats:italic>\n                    <\/jats:bold>\n                    Over the past decade it has become clear that Trx-1 is not only critical for tumor functions, which has resulted in therapeutic approaches targeting this protein, but also essential for proper functions of the vasculature and the heart. Changes in post-translational modifications of Trx-1 or in its interactions with other proteins can lead to a switch from a physiologic state of cells and organs to diverse pathologies. This review provides insights into the role of Trx-1 in different physiological situations and cardiac hypertrophy, ischemia reperfusion injury, heart failure, atherosclerosis, and diabetes mellitus type 2, underscoring the central role of Trx-1 in cardiovascular health and disease.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Future Directions:<\/jats:italic>\n                    <\/jats:bold>\n                    Thus, the manipulation of Trx-1 activity in the heart and\/or vasculature, for example, by small molecules, seems to be a promising therapeutic option in cardiovascular diseases, as general anti-oxidant treatments would not take into account interactions of Trx-1 with other proteins and also eliminate vital ROS.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    18, 1053\u20131062.\n                  <\/jats:p>","DOI":"10.1089\/ars.2012.4822","type":"journal-article","created":{"date-parts":[[2012,8,7]],"date-time":"2012-08-07T08:21:36Z","timestamp":1344327696000},"page":"1053-1062","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":42,"title":["Interacting with Thioredoxin-1\u2014Disease or No Disease?"],"prefix":"10.1177","volume":"18","author":[{"given":"Tim-Christian","family":"Zschauer","sequence":"first","affiliation":[{"name":"University of Duesseldorf gGmbH","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shouji","family":"Matsushima","sequence":"additional","affiliation":[{"name":"University of Medicine and Dentistry of New Jersey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joachim","family":"Altschmied","sequence":"additional","affiliation":[{"name":"University 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