{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:39:05Z","timestamp":1772159945636,"version":"3.50.1"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2025,12,5]],"date-time":"2025-12-05T00:00:00Z","timestamp":1764892800000},"content-version":"vor","delay-in-days":1464,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2021,12,2]],"date-time":"2021-12-02T00:00:00Z","timestamp":1638403200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP18K07046"],"award-info":[{"award-number":["JP18K07046"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP18K07046"],"award-info":[{"award-number":["JP18K07046"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Cardiac ischaemia\/reperfusion (I\/R) injury remains a critical issue in the therapeutic management of ischaemic heart failure. Although mild hypothermia has a protective effect on cardiac I\/R injury, more rapid and safe methods that can obtain similar results to hypothermia therapy are required. 2-Methyl-2-thiazoline (2MT), an innate fear inducer, causes mild hypothermia resulting in resistance to critical hypoxia in cutaneous or cerebral I\/R injury. The aim of this study is to demonstrate the protective effect of systemically administered 2MT on cardiac I\/R injury and to elucidate the mechanism underlying this effect.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>A single subcutaneous injection of 2MT (50 mg\/kg) was given prior to reperfusion of the I\/R injured 10 week-old male mouse heart and its efficacy was evaluated 24 h after the ligation of the left anterior descending coronary artery. 2MT preserved left ventricular systolic function following I\/R injury (ejection fraction, %: control 37.9 \u00b1 6.7, 2MT 54.1 \u00b1 6.4, P &amp;lt; 0.01). 2MT also decreased infarct size (infarct size\/ischaemic area at risk, %: control 48.3 \u00b1 12.1, 2MT 25.6 \u00b1 4.2, P &amp;lt; 0.05) and serum cardiac troponin levels (ng\/mL: control 8.9 \u00b1 1.1, 2MT 1.9 \u00b1 0.1, P &amp;lt; 0.01) after I\/R. Moreover, 2MT reduced the oxidative stress-exposed area within the heart (%: control 25.3 \u00b1 4.7, 2MT 10.8 \u00b1 1.4, P &amp;lt; 0.01). These results were supported by microarray analysis of the mouse hearts. 2MT induced a transient, mild decrease in core body temperature (\u00b0C: \u22122.4 \u00b1 1.4), which gradually recovered over several hours. Metabolome analysis of the mouse hearts suggested that 2MT minimized energy metabolism towards suppressing oxidative stress. Furthermore, 18F-fluorodeoxyglucose-positron emission tomography\/computed tomography imaging revealed that 2MT reduced the activity of brown adipose tissue (standardized uptake value: control 24.3 \u00b1 6.4, 2MT 18.4 \u00b1 5.8, P &amp;lt; 0.05). 2MT also inhibited mitochondrial respiration and glycolysis in rat cardiomyoblasts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We identified the cardioprotective effect of systemically administered 2MT on cardiac I\/R injury by sparing energy metabolism with reversible hypothermia. Our results highlight the potential of drug-induced hypothermia therapy as an adjunct to coronary intervention in severe ischaemic heart disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.13732","type":"journal-article","created":{"date-parts":[[2021,12,2]],"date-time":"2021-12-02T03:43:57Z","timestamp":1638416637000},"page":"428-441","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Energy-Sparing by 2-Methyl-2-Thiazoline Protects Heart from Ischaemia\/Reperfusion Injury"],"prefix":"10.1093","volume":"9","author":[{"given":"Masahiro","family":"Nishi","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine , Kyoto ,","place":["Japan"]},{"name":"Cardiovascular Branch, National Heart, Lung and Blood Institute, National Institutes of Health , Bethesda, MD 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