Kougias Panagiotis, Chai Hong, Lin Peter H, Yao Qizhi, Lumsden Alan B, Chen Changyi
Molecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030, USA.
J Surg Res. 2005 Jun 1;126(1):121-9. doi: 10.1016/j.jss.2004.12.023.
Adipose tissue has recently emerged as an active endocrine organ that secretes a variety of metabolically important substances, collectively called adipocytokines or adipokines. In this review we summarize the effects of the adipokines leptin, adiponectin, and resistin on the vasculature and their potential role for pathogenesis of vascular disease. Leptin is associated with arterial wall thickness, decreased vessel distensibility, and elevated C reactive protein (CRP) levels. Leptin possesses procoagulant and antifibrinolytic properties, and it promotes thrombus and atheroma formation, probably through the leptin receptors by promoting vascular inflammation, proliferation, and calcification, and by increasing oxidative stress. Research for development of pharmacologic antagonism for the leptin receptor is currently under way. Adiponectin inhibits the expression of the adhesion molecules ICAM-1, VCAM-1, and P selectin. Therefore, it interferes with monocyte adherence to endothelial cells and their subsequent migration to the subendothelial space, one of the initial events in the development of atherosclerosis. Adiponectin also inhibits the transformation of macrophages to foam cells in vitro and decreases their phagocytic activity. Resistin, discovered in 2001, represents the newest of the adipokines and was named for its ability to promote insulin resistance. Resistin increases the expression of the adhesion molecules VCAM-1 and ICAM-1, up-regulates the monocyte chemoattractant chemokine-1, and promotes endothelial cell activation via ET-1 release. Although many aspects of its function need further clarification, it appears that resistin will add significantly to our knowledge of the pathophysiology of vascular disease and the metabolic syndrome.
脂肪组织最近已成为一个活跃的内分泌器官，它分泌多种对代谢具有重要意义的物质，这些物质统称为脂肪细胞因子或脂联素。在本综述中，我们总结了瘦素、脂联素和抵抗素这几种脂肪细胞因子对脉管系统的影响及其在血管疾病发病机制中的潜在作用。瘦素与动脉壁厚度增加、血管扩张性降低以及C反应蛋白（CRP）水平升高有关。瘦素具有促凝和抗纤溶特性，它可能通过促进血管炎症、增殖和钙化以及增加氧化应激，经瘦素受体促进血栓和动脉粥样硬化斑块形成。目前正在开展针对瘦素受体的药物拮抗研究。脂联素可抑制细胞间黏附分子1（ICAM - 1）、血管细胞黏附分子1（VCAM - 1）和P选择素等黏附分子的表达。因此，它会干扰单核细胞与内皮细胞的黏附及其随后向内皮下间隙的迁移，而这是动脉粥样硬化发展过程中的初始事件之一。脂联素在体外还可抑制巨噬细胞向泡沫细胞的转化并降低其吞噬活性。抵抗素于2001年被发现，是最新发现的脂肪细胞因子，因其促进胰岛素抵抗的能力而得名。抵抗素可增加黏附分子VCAM - 1和ICAM - 1的表达，上调单核细胞趋化因子 - 1，并通过内皮素 - 1（ET - 1）释放促进内皮细胞活化。尽管其功能的许多方面仍需进一步阐明，但抵抗素似乎将极大地增进我们对血管疾病和代谢综合征病理生理学的认识。
