Department of Pharmacology and Nutritional Sciences, Saha Cardiovascular Research Center, and Barnstable Brown Diabetes Center, University of Kentucky, 553 Wethington Building, 900 South Limestone, Lexington, KY, 40536-0200, USA.
Curr Atheroscler Rep. 2021 Jan 15;23(2):7. doi: 10.1007/s11883-020-00901-4.
Serum amyloid A (SAA) is a highly sensitive acute phase reactant that has been linked to a number of chronic inflammatory diseases. During a systemic inflammatory response, liver-derived SAA is primarily found on high-density lipoprotein (HDL). The purpose of this review is to discuss recent literature addressing the pathophysiological functions of SAA and the significance of its association with HDL.
Studies in gene-targeted mice establish that SAA contributes to atherosclerosis and some metastatic cancers. Accumulating evidence indicates that the lipidation state of SAA profoundly affects its bioactivities, with lipid-poor, but not HDL-associated, SAA capable of inducing inflammatory responses in vitro and in vivo. Factors that modulate the equilibrium between lipid-free and HDL-associated SAA have been identified. HDL may serve to limit SAA's bioactivities in vivo. Understanding the factors leading to the release of systemic SAA from HDL may provide insights into chronic disease mechanisms.
血清淀粉样蛋白 A（SAA）是一种高度敏感的急性期反应物，与许多慢性炎症性疾病有关。在全身炎症反应中，肝脏来源的 SAA主要存在于高密度脂蛋白（HDL）上。本文综述的目的是讨论最近关于 SAA 的病理生理学功能及其与 HDL 相关意义的文献。
基因靶向小鼠的研究表明，SAA 有助于动脉粥样硬化和一些转移性癌症。越来越多的证据表明，SAA 的脂质化状态对其生物活性有深远影响，只有脂质缺乏的 SAA，而不是与 HDL 相关的 SAA，能够在体外和体内诱导炎症反应。已经确定了调节游离脂质和与 HDL 相关的 SAA 之间平衡的因素。HDL 可能有助于限制 SAA 在体内的生物活性。了解导致系统性 SAA 从 HDL 释放的因素可能有助于深入了解慢性疾病的机制。
