精氨酸酶
炎症
巨噬细胞
鸟氨酸
一氧化氮
精氨酸
细胞生物学
下调和上调
受体
伤口愈合
生物
化学
癌症研究
生物化学
免疫学
内分泌学
基因
氨基酸
体外
作者
Benoît Pourcet,Inés Pineda-Torra
标识
DOI:10.1016/j.tcm.2012.10.003
摘要
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.
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