AMPK: An Ambiguous Position for Atrial Fibrillation
AMPK: An Ambiguous Position for Atrial Fibrillation
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AMPK：心房颤动的模糊定位
DOI：
10.1016/j.tem.2018.02.009
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发表时间：
2018-06
期刊：
影响因子：
--
通讯作者：
Qiming Liu
中科院分区：
文献类型：
--
作者：
Jiayi Li;Fan Bai;Biao Li;Qiming Liu
我们怀着极大的兴趣阅读了Day及其同事题为“AMPK作为治疗代谢性疾病的治疗靶点”的综述。在他们的综述中，他们证明了amp激活的蛋白激酶（AMPK）活性促进抗炎表型，防止肥胖诱导的胰岛素抵抗，防止肝脏脂质积累，并维持各种细胞类型（如肝细胞、巨噬细胞和脂肪细胞）的线粒体功能。这一信息无疑将有助于指导ampk靶向治疗慢性代谢疾病的发展。如上所述，AMPK似乎具有积极的内在特征。目前越来越多的研究也证明AMPK可能在心脏电生理和心律失常[2]中具有潜在的作用。此外，AMPK可引起脂质积累，减少葡萄糖摄取，增加糖原合成，这些与预期相反，促进了能量供应的不平衡。此外，AMPK的激活似乎介导了节律不规律的肌细胞的代谢变化，因为在化合物c（一种细胞渗透性atp竞争性AMPK抑制剂）存在下进行的实验，导致FAT-CD36和GLUT-4的上调，这种代谢重塑可能在一定程度上促进了心房颤动（AF）的病理。
We have read with great interest the review of Day and colleagues entitled ‘AMPK as a Therapeutic Target for Treating Metabolic Diseases’[1]. In their review, they demonstrate that AMP-activated protein kinase (AMPK) activity promotes an anti-inflammatory phenotype, protects against obesity-induced insulin resistance, prevents liver lipid accumulation, and maintains mitochondrial function in various cell types such as hepatocytes, macrophages, and adipocytes. This information will certainly be useful in guiding the development of AMPK-targeted therapeutics to treat chronic metabolic diseases. As was noted above, AMPK appears to possess a positive intrinsic characteristic. Current accumulating research has also provided evidence that AMPK might have a potential role in cardiac electrophysiology and arrhythmia [2]. In addition, AMPK can cause lipid accumulation, reduce glucose uptake, and increase glycogen synthesis, and these promote the imbalance of energy supply contrary to expectations. Furthermore, AMPK activation appears to mediate the metabolic change in irregularly paced myocytes, as experiments conducted in the presence of Compound c, a cell-permeable ATP-competitive AMPK inhibitor, result in [47_TD $ DIFF] upregulation of FAT-CD36 and GLUT-4, and this metabolic remodeling may contribute in part to the pathology of atrial fibrillation (AF)[3].
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