{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T22:30:13Z","timestamp":1790721013692,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2018,6,25]],"date-time":"2018-06-25T00:00:00Z","timestamp":1529884800000},"content-version":"vor","delay-in-days":175,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81701891"],"award-info":[{"award-number":["81701891"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81201458"],"award-info":[{"award-number":["81201458"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81671891"],"award-info":[{"award-number":["81671891"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81471844"],"award-info":[{"award-number":["81471844"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2018,1]]},"abstract":"<jats:p>\n                    Patients with diabetes are more vulnerable to myocardial ischemia\/reperfusion (MI\/R) injury, which is associated with excessive reactive oxygen species (ROS) generation and decreased antioxidant defense. Histone deacetylase 6 (HDAC6), a regulator of the antioxidant protein peroxiredoxin 1 (Prdx1), is associated with several pathological conditions in the cardiovascular system. This study investigated whether tubastatin A (TubA), a highly selective HDAC6 inhibitor, could confer a protective effect by modulating Prdx1 acetylation in a rat model of MI\/R and an\n                    <jats:italic>in vitro<\/jats:italic>\n                    model of hypoxia\/reoxygenation (H\/R). Here, we found that diabetic hearts with excessive HDAC6 activity and decreased acetylated\u2010Prdx1 levels were more vulnerable to MI\/R injury. TubA treatment robustly improved cardiac function, reduced cardiac infarction, attenuated ROS generation, and increased acetylated\u2010Prdx1 levels in diabetic MI\/R rats. These results were further confirmed by an\n                    <jats:italic>in vitro<\/jats:italic>\n                    study using H9c2 cells. Furthermore, a study using Prdx1 acetyl\u2010silencing mutants (K197R) showed that TubA only slightly attenuated H\/R\u2010induced cell death and ROS generation in K197R\u2010transfected H9c2 cells exposed to high glucose (HG), but these differences were not statistically significant. Taken together, these findings suggest that HDAC6 inhibition reduces ROS generation and confers a protective effect against MI\/R or H\/R injury by modulating Prdx1 acetylation at K197.\n                  <\/jats:p>","DOI":"10.1155\/2018\/9494052","type":"journal-article","created":{"date-parts":[[2018,6,25]],"date-time":"2018-06-25T19:33:00Z","timestamp":1529955180000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":101,"title":["Inhibition of HDAC6 Activity Alleviates Myocardial Ischemia\/Reperfusion Injury in Diabetic Rats: Potential Role of Peroxiredoxin 1 Acetylation and Redox 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