Fibroblast growth factor-2-induced cardioprotection against myocardial infarction occurs via the interplay between nitric oxide, protein kinase signaling, and ATP-sensitive potassium channels.
Fibroblast growth factor-2-induced cardioprotection against myocardial infarction occurs via the interplay between nitric oxide, protein kinase signaling, and ATP-sensitive potassium channels.
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DOI：
10.3109/08977194.2012.656759
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发表时间：
2012-04
期刊：
影响因子：
--
通讯作者：
Schultz Jel J
中科院分区：
文献类型：
--
作者：
Manning JR;Carpenter G;Porter DR;House SL;Pietras DA;Doetschman T;Schultz Jel J
成纤维细胞生长因子 2 (FGF2) 通过庞大的蛋白激酶网络保护心脏免受缺血再灌注 (I-R) 损伤。在心脏中，这些 FGF2 触发信号的下游效应器尚未确定。据推测，一氧化氮 (NO) 信号传导和 ATP 敏感钾 (KATP) 通道活性是 FGF2 介导的心脏保护作用激活的蛋白激酶的关键效应器。在缺乏或存在 NO 合酶 (NOS) 同种型或肌膜 (sarcKATP) 和线粒体 (mitoKATP) KATP 通道选择性抑制剂的情况下，心脏特异性过度表达 FGF2 (FGF2 Tg) 的心脏会遭受 I-R 损伤。多种 NOS 亚型对于 FGF2 介导的心脏保护是必需的，并且在抑制蛋白激酶 C 或丝裂原激活的蛋白激酶后，FGF2 Tg 心脏中的亚硝酸盐水平显着降低。同样，sarcKATP 和 mitoKATP 通道对于内源性 FGF2 引起的心脏保护也很重要。这些发现表明 FGF2 诱导的心脏保护作用是通过蛋白激酶-NOS 途径以及 KATP 通道活性发生的。
Fibroblast growth factor-2 (FGF2) protects the heart from ischemia–reperfusion (I-R) injury via a vast network of protein kinases. In the heart, downstream effectors of these FGF2-triggered signals have not yet been identified. It is hypothesized that nitric oxide (NO) signaling and ATP-sensitive potassium (KATP) channel activity are key effectors of protein kinases activated by FGF2-mediated cardioprotection. Hearts with a cardiac-specific overexpression of FGF2 (FGF2 Tg) were subjected to I-R injury in the absence or the presence of selective inhibitors of NO synthase (NOS) isoforms or sarcolemmal (sarcKATP) and mitochondrial (mitoKATP) KATP channels. Multiple NOS isoforms are necessary for FGF2-mediated cardioprotection, and nitrite levels are significantly reduced in FGF2 Tg hearts upon inhibition of protein kinase C or mitogen-activated protein kinases. Likewise, sarcKATP and mitoKATP channels are important for cardioprotection elicited by endogenous FGF2. These findings suggest that FGF2-induced cardioprotection occurs via protein kinase-NOS pathways as well as KATP channel activity.
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DOI：
10.1111/j.1440-1681.2011.05550.x
发表时间：
2011-10-01
影响因子：
2.9
作者：
Bai, Yushan;Muqier;Minatoguchi, Shinya
通讯作者：
Minatoguchi, Shinya
影响因子：
4.8
作者：
Favata, MF;Horiuchi, KY;Trzaskos, JM
通讯作者：
Trzaskos, JM
影响因子：
56.9
作者：
CUEVAS, P;CARCELLER, F;GIMENEZGALLEGO, G
通讯作者：
GIMENEZGALLEGO, G
影响因子：
4.8
作者：
Adak, S;Santolini, J;Stuehr, DJ
通讯作者：
Stuehr, DJ
影响因子：
20.1
作者：
Baines, CP;Song, CX;Ping, PP
通讯作者：
Ping, PP