Rojas Edward, Rodríguez-Molina Daloha, Bolli Peter, Israili Zafar H, Faría Judith, Fidilio Enzamaría, Bermúdez Valmore, Velasco Manuel
Endocrine and Metabolic Diseases Research Center "Dr. Félix Gómez", University of Zulia, Maracaibo, Venezuela,
Curr Hypertens Rep. 2014 Aug;16(8):463. doi: 10.1007/s11906-014-0463-7.
It has been two decades since the discovery of adiponectin, and today its role in insulin resistance, inflammation, and atherosclerosis are areas of major interest. Production of adiponectin is reduced in all inflammatory processes and states of insulin resistance such as obesity, type 2 diabetes mellitus, and coronary artery disease. Adiponectin regulates carbohydrate metabolism, and may also regulate vascular homeostasis by affecting important signaling pathways in endothelial cells and modulating inflammatory responses in the subendothelial space. Clinical studies have demonstrated a relationship between serum adiponectin concentrations and the activity of the renin-angiotensin-aldosterone system (RAAS), causing changes in blood pressure. Antihypertensive therapy with angiotensin II receptor blockers (ARBs) has been demonstrated to increase adiponectin levels in 3-6 months. Adiponectin has also been shown to play a role in cardiac injury in modulation of pro-survival reactions, cardiac energy metabolism, and inhibition of hypertrophic remodeling. The effects of adiponectin on the cardiovascular system are believed to be partially mediated by the activation of 5' adenosine monophosphate-activated protein kinase (AMPK) and cyclooxygenase-2 (COX-2) pathways, reducing endothelial cell apoptosis, promoting nitric oxide production, decreasing tumor necrosis factor-alpha (TNF-α) activity, and preventing atherosclerotic proliferation and smooth muscle cell migration. Further evaluation of biologically active forms of adiponectin and its receptor should help to clarify how obesity affects the cardiovascular system.
自脂联素被发现以来已有二十年，如今它在胰岛素抵抗、炎症和动脉粥样硬化中的作用是主要研究热点。在所有炎症过程以及胰岛素抵抗状态（如肥胖、2型糖尿病和冠状动脉疾病）中，脂联素的产生都会减少。脂联素调节碳水化合物代谢，还可能通过影响内皮细胞中的重要信号通路以及调节内皮下空间的炎症反应来调节血管稳态。临床研究表明血清脂联素浓度与肾素 - 血管紧张素 - 醛固酮系统（RAAS）的活性之间存在关联，进而导致血压变化。使用血管紧张素II受体阻滞剂（ARBs）进行的抗高血压治疗已被证明在3至6个月内可提高脂联素水平。脂联素还被证明在心脏损伤中对生存反应调节、心脏能量代谢以及抑制肥厚性重塑方面发挥作用。脂联素对心血管系统的影响被认为部分是通过激活5' 腺苷单磷酸激活蛋白激酶（AMPK）和环氧合酶 - 2（COX - 2）途径介导的，可减少内皮细胞凋亡、促进一氧化氮生成、降低肿瘤坏死因子 - α（TNF - α）活性，并防止动脉粥样硬化增殖和平滑肌细胞迁移。对脂联素及其受体的生物活性形式进行进一步评估应有助于阐明肥胖如何影响心血管系统。
