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Functional role of the transient receptor potential canonical (TRPC) channels in the development of cardiac ischemia/reperfusion injury

Functional role of the transient receptor potential canonical (TRPC) channels in the development of cardiac ischemia/reperfusion injury
瞬时受体电位经典(TRPC)通道在心脏缺血/再灌注损伤发展中的功能作用
批准号:
22590205
负责人:
MATSUURA Hiroshi
金额:
$2.83万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2010
资助国家:
日本
项目状态:
已结题
起止时间:
2010 至 2012

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中文摘要
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英文摘要
Ca2+overload has been implicated in the pathogenesis of ischemia/reperfusion injury in the heart. The present investigation used Langendorff perfusion method of mouse hearts and fluorescence Ca2+imaging of mouse ventricular myocytes and revealed that the transient receptor potential canonical (TRPC) channels mediate the Ca2+entry responsible for Ca2+overload during the reperfusion of ischemic myocardium. These observations indicate that TRPC channel blockade could provide potential new avenues to develop strategies for protecting the heart during reperfusion of ischemic myocardium.
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Sevoflurane protects ventricular myocytes from Ca2+paradox-mediated Ca2+overload by blocking the activation of transient receptor potential canonical channels
七氟烷通过阻断瞬时受体电位经典通道的激活,保护心室肌细胞免受 Ca2 悖论介导的 Ca2 超载
DOI: 10.1097/aln.0b013e31822b7901
发表时间: 2011
期刊: Anesthesiology
影响因子: 8.8
作者: [Kojima A, Kitagawa H, Omatsu-Kanbe M,Matsuura H, Nosaka S]
通讯作者: Nosaka S
Nosaka S. Sevoflurane protects cardiomyocyte from Ca2+paradox by preserving SR Ca2+and blocking TRPC channel
Nosaka S.七氟烷通过保留 SR Ca2 并阻断 TRPC 通道来保护心肌细胞免受 Ca2 悖论
DOI: --
发表时间: 2010
期刊:
影响因子: --
作者: [Kojima A, Kitagawa H, Omatsu-Kanbe M, Matsuura H]
通讯作者: Matsuura H
DOI: 10.1111/j.1476-5381.2010.00986.x
发表时间: 2010-12-01
期刊: BRITISH JOURNAL OF PHARMACOLOGY
影响因子: 7.3
作者: [Kojima, Akiko, Kitagawa, Hirotoshi, Nosaka, Shuichi]
通讯作者: Nosaka, Shuichi
COX-2 selective blocker inhibits the TNF-induced apoptosis in isolated rabbit articular chondrocytes.
COX-2 选择性阻滞剂抑制 TNF 诱导的兔离体关节软骨细胞凋亡。
DOI: --
发表时间: 2013
期刊:
影响因子: --
作者: [Kumagai K, Imai S, Toyoda F, Maeda T, Kubo M, Matsuura H, Matsusue Y]
通讯作者: Matsusue Y
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