期刊
TRENDS IN CARDIOVASCULAR MEDICINE
卷 23, 期 5, 页码 143-152出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcm.2012.10.003
关键词
-
资金
- Medical Research Council (New Investigator Grant) [G0801278]
- E.U. International Reintegration Program [PIRG02-GA-2007-224867]
- Medical Research Council [G0801278] Funding Source: researchfish
- MRC [G0801278] Funding Source: UKRI
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 omithine, 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. (c) 2013 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据