Centre for Clinical Pharmacology, Division of Medicine, University College London, London WC1E6JJ, UK.
Trends Cardiovasc Med. 2013 Jul;23(5):143-52. doi: 10.1016/j.tcm.2012.10.003. Epub 2013 Jan 30.
Atherosclerosis results from a metabolic imbalance and chronic arterial inflammation and macrophages are key during the initiation and progression of atherosclerotic lesions. A number of macrophage subsets have been identified in atherosclerotic plaques. Arginase 1 (Arg1), a marker for the M2 anti-inflammatory subset, hydrolyzes l-arginine into urea and ornithine, a precursor to l-proline and polyamines, which are implicated in tissue repair and wound healing. Additionally, Arg1 inhibits nitric oxide-mediated inflammatory pathways by competing with iNOS for the same substrate, l-arginine. Therefore, changes in Arg1 expression in macrophages may affect the development of atherosclerosis. Here, we present an overview of the transcriptional regulation of macrophage Arg1, focusing on the nuclear receptor family of ligand-activated transcription factors, and the relevance of this regulation to atherosclerosis.
动脉粥样硬化是由代谢失衡和慢性动脉炎症引起的，而巨噬细胞在动脉粥样硬化病变的发生和发展中起着关键作用。在动脉粥样硬化斑块中已经鉴定出许多巨噬细胞亚群。精氨酸酶 1（Arg1）是 M2 抗炎亚群的标志物，它将 l-精氨酸水解为尿素和鸟氨酸，鸟氨酸是 l-脯氨酸和多胺的前体，多胺参与组织修复和伤口愈合。此外，Arg1 通过与 iNOS 竞争相同的底物 l-精氨酸来抑制一氧化氮介导的炎症途径。因此，巨噬细胞中 Arg1 的表达变化可能会影响动脉粥样硬化的发展。在这里，我们概述了巨噬细胞 Arg1 的转录调控，重点介绍了配体激活转录因子的核受体家族，以及这种调控与动脉粥样硬化的相关性。
