Abstract:
BACKGROUND:Myocardial infarction (MI) is one of the most common causes of cardiac morbidity and mortality. Many evidences suggest that hypothermia have a more pronounced impact as an adjunctive therapy for MI to reduce infarct size. However, the function of long non-coding RNAs (lncRNA) in therapeutic hypothermia for MI remains poorly understood. METHODS:In this study, we investigated the expression of lncRNA-UIHTC (upregulated in hypothermia treated cardiomyocytes, NONHSAT094064) in ischemic heart tissues. To investigate its function, overexpression of UIHTC was performed by adeno-associated virus vectors after MI model in rat. RESULTS:lncRNA-UIHTC was upregulated in ischemic or injury cardiomyocytes. Overexpression of lncRNA-UIHTC in peri-infarction attenuated cardiac dysfunction in vivo. Mechanistically, lncRNA-UIHTC enhanced the mitochondrial function via upregulation of PGC1α. Moreover, when we knocked down PGC1α, the mitochondrial maximal oxygen consumption and ATP levels enhanced by overexpression of UIHTC were nearly completely restored. CONCLUSIONS:Altogether we have provided a new mechanism whereby hypothermia protected heart against ischemic via lncRNA-UIHTC. The UIHTC provided a new potential therapeutic target for MI but prevented the complications of hypothermia.
journal_name
Int J Cardioljournal_title
International journal of cardiologyauthors
Zhang J,Yu L,Xu Y,Liu Y,Li Z,Xue X,Wan S,Wang Hdoi
10.1016/j.ijcard.2017.12.097subject
Has Abstractpub_date
2018-09-01 00:00:00pages
213-217eissn
0167-5273issn
1874-1754pii
S0167-5273(17)35903-Xjournal_volume
266pub_type
杂志文章abstract:BACKGROUND:Although diabetes is associated with poor clinical outcomes after acute myocardial infarction, to date there have been no reports focusing on the myocardial oxygen metabolism in these patients. Thus, we evaluated the myocardial oxygen metabolism in patients with and without diabetes suffering from acute myoc...
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pub_type: 临床试验,杂志文章,随机对照试验
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pub_type: 杂志文章,多中心研究,随机对照试验
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pub_type: 杂志文章,评审
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更新日期:2009-06-26 00:00:00