The effects of aging on apoptosis following myocardial infarction.
The effects of aging on apoptosis following myocardial infarction.
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DOI：
10.1111/1755-5922.12043
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发表时间：
2013-12
影响因子：
3.1
通讯作者：
Lee RJ
中科院分区：
文献类型：
--
作者：
Boyle AJ;Hwang J;Ye J;Shih H;Jun K;Zhang Y;Fang Q;Sievers R;Yeghiazarians Y;Lee RJ
年龄与心肌梗死（MI）后心力衰竭和死亡的发生率较高相关。导致这些更糟糕结果的分子和细胞变化尚不清楚。年轻和老龄小鼠通过LAD结扎诱导MI。衰老小鼠的死亡率显著增加。年轻和老年心肌梗死后的心脏都没有诱发室性心动过速。心肌细胞凋亡在年轻和老龄小鼠MI后早期增加，但在老龄小鼠中程度更大。用Ac-DEVD-CHO抑制胱天蛋白酶导致年轻小鼠心肌细胞中活化的胱天蛋白酶3减少61%和细胞凋亡减少84%（p<0.05），但在衰老小鼠中没有。基因通路分析表明，在MI后衰老小鼠中，caspase和Map 3 k1/Mapk 10通路都被激活，这可能有助于它们对caspase抑制的抵抗。衰老的心脏激活不同的凋亡途径，有更多的心肌细胞凋亡，并抵抗MI后的抗凋亡治疗。可能需要新的或联合方法来改善老年患者MI后的结局。
Aging is associated with higher incidence of heart failure and death following myocardial infarction (MI). The molecular and cellular changes that lead to these worse outcomes are not known. Young and aging mice underwent induction of MI by LAD ligation. There was a significant increase in mortality in the aging mice. Neither the young nor aging hearts after MI had inducible ventricular tachycardia. Cardiomyocyte apoptosis increases early after MI in young and aging mice, but to a much greater degree in the aging mice. Caspase inhibition with Ac-DEVD-CHO resulted in a 61% reduction in activated caspase 3 and an 84% reduction in apoptosis in cardiomyocytes in young mice (p<0.05), but not in aging mice. Gene pathway profiling demonstrated activation of both the caspase and Map3k1/Mapk10 pathways in aging mice following MI, which may contribute to their resistance to caspase inhibition. Aging hearts activate distinct apoptotic pathways, have more cardiomyocyte apoptosis, and are resistant to anti-apoptotic therapies following MI. Novel or combination approaches may be required to improve outcomes in aging patients following MI.
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DOI：
10.1152/ajpheart.00206.2001
发表时间：
2002-02-01
影响因子：
4.8
作者：
Gould, KE;Taffet, GE;Entman, ML
通讯作者：
Entman, ML
影响因子：
10.8
作者：
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Hock, CE
影响因子：
3.9
作者：
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通讯作者：
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影响因子：
12.3
作者：
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通讯作者：
Zhang J
影响因子：
20.1
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通讯作者：
Hare JM