Li Li, Wu Li-Ling
Department of Physiology and Pathophysiology, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University Health Science Center, Beijing 100083, China.
Sheng Li Xue Bao. 2007 Oct 25;59(5):614-8.
Adiponectin, derived mainly from white adipose tissue, regulates glucose and fatty acid metabolism and has anti-inflammatory and anti-atherosclerotic properties. The decrease in plasma adiponectin concentration contributes to the development of metabolic and cardiovascular diseases. AMP-activated protein kinase (AMPK) is a serine/threonine kinase which plays an important role in regulating many cellular processes, particularly pathways involved in cellular energy status. AMPK is now recognized as a fuel gauge in mammalian cells. Adiponectin activates AMPK phosphorylation and then promotes ATP-generating pathways in heart, including glucose transport, glycolysis, and fatty acid oxidation. The recent evidence has shown that AMPK activation has an important role in the vasculature where it may exert anti-atherosclerotic effects. Phosphorylation of AMPK induced by adiponectin inhibits protein synthesis, and may be an adaptive response to pathological cardiac hypertrophy. AMPK also has a cardioprotective role against myocardial injury and apoptosis in the ischemic heart. This review will discuss the role of AMPK in adiponectin-mediated protective properties of cardiovascular diseases.
脂联素主要来源于白色脂肪组织,可调节葡萄糖和脂肪酸代谢,并具有抗炎和抗动脉粥样硬化特性。血浆脂联素浓度降低会促使代谢性疾病和心血管疾病的发生。AMP激活的蛋白激酶(AMPK)是一种丝氨酸/苏氨酸激酶,在调节许多细胞过程中发挥重要作用,尤其是参与细胞能量状态的途径。AMPK现在被认为是哺乳动物细胞中的能量传感器。脂联素激活AMPK磷酸化,进而促进心脏中产生ATP的途径,包括葡萄糖转运、糖酵解和脂肪酸氧化。最近的证据表明,AMPK激活在血管系统中具有重要作用,可能发挥抗动脉粥样硬化作用。脂联素诱导的AMPK磷酸化抑制蛋白质合成,可能是对病理性心肌肥大的一种适应性反应。AMPK对缺血性心脏的心肌损伤和细胞凋亡也具有心脏保护作用。本综述将讨论AMPK在脂联素介导的心血管疾病保护特性中的作用。