Remote Liver Ischemic Preconditioning Protects against Sudden Cardiac Death via an ERK/GSK-3β-Dependent Mechanism.
Remote Liver Ischemic Preconditioning Protects against Sudden Cardiac Death via an ERK/GSK-3β-Dependent Mechanism.
复制标题
远程肝脏缺血预处理通过 ERK/GSK-3beta 依赖性机制防止心脏性猝死。
DOI：
10.1371/journal.pone.0165123
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Abbott GW
中科院分区：
文献类型：
--
作者：
Hu Z;Hu S;Yang S;Chen M;Zhang P;Liu J;Abbott GW
Preconditioning stimuli conducted in remote organs can protect the heart against subsequent ischemic injury, but effects on arrhythmogenesis and sudden cardiac death (SCD) are unclear. Here, we investigated the effect of remote liver ischemia preconditioning (RLIPC) on ischemia/reperfusion (I/R)-induced cardiac arrhythmia and sudden cardiac death (SCD) in vivo, and determined the potential role of ERK/GSK-3βsignaling. Male Sprague Dawley rats were randomized to sham-operated, control, or RLIPC groups. RLIPC was induced by alternating four 5-minute cycles of liver ischemia with 5-minute intermittent reperfusions. To investigate I/R-induced arrhythmogenesis, hearts in each group were subsequently subjected to 5-minute left main coronary artery ligation followed by 20-minute reperfusion. RLIPC reduced post-I/R ventricular arrhythmias, and decreased the incidence of SCD >threefold. RLIPC increased phosphorylation of cardiac ERK1/2, and GSK-3β Ser9 but not Tyr216 post-I/R injury. Inhibition of either GSK-3β (with SB216763) or ERK1/2 (with U0126) abolished RLIPC-induced antiarrhythmic activity and GSK-3β Ser9 and ERK1/2 phosphorylation, leaving GSK-3β Tyr216 phosphorylation unchanged. RLIPC exerts a powerful antiarrhythmic effect and reduces predisposition to post-IR SCD. The underlying mechanism of RLIPC cardioprotection against I/R-induced early arrhythmogenesis may involve ERK1/2/GSK-3β Ser9-dependent pathways.
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DOI：
10.1161/circgenetics.113.000315
发表时间：
2014-02
期刊：
Circulation. Cardiovascular genetics
影响因子：
--
作者：
Hu Z;Kant R;Anand M;King EC;Krogh-Madsen T;Christini DJ;Abbott GW
通讯作者：
Abbott GW
影响因子：
8.9
作者：
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通讯作者：
Stevenson, William G.
影响因子：
37.8
作者：
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通讯作者：
REIMER, KA
DOI：
10.1111/j.1540-8167.2012.02397.x
发表时间：
2012-12-01
影响因子：
2.7
作者：
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通讯作者：
Kloner, Robert A.
影响因子：
9.5
作者：
Mortensen, UM;Norgaard, BL;Nielsen, TT
通讯作者：
Nielsen, TT