期刊
EUROPEAN HEART JOURNAL
卷 33, 期 16, 页码 2025-2034出版社
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehs175
关键词
Atherosclerosis; 3-Hydroxyanthranilic acid; Tryptophan; Lipid metabolism; Indoleamine-2; 3-deoxygenase (IDO)
资金
- CERIC Linnaeus Program
- Swedish Research Council-Medicine [521-2009-4203, 349-2007-8703]
- Swedish Heart-Lung Foundation
- Swedish Foundation for Strategic Research-SSF
- Vinnova Foundation
- Combine
- Stiftelsen for Gamla Tjanarinnor
- O.E. och Edla Johanssons vetenskapliga stiftelse
- Stiftelsen for alderssjukdomar - KI
- Loo och Hans Ostermans stiftelse
- Stiftelsen Professor Nanna Svartz fond
- KI fond
- European Union projects (Molstroke, AtheroRemo)
Cardiovascular disease is the most common cause of death in the world and atherosclerosis, an inflammatory process in the vessel wall, accounts for the majority of these deaths. The tryptophan metabolite 3-hydroxyanthranilic acid (3-HAA) has been shown to inhibit inflammation in different experimental autoimmune disease models. However, the effect of 3-HAA in atherosclerosis has never been explored. In this study, we used the atherosclerosis prone Ldlr/ mice, and cell culture experiments to evaluate the role of 3-HAA in atherosclerosis. Eight weeks treatment with 3-HAA significantly reduced the lesion size in the aorta, and modulated local and systemic inflammatory responses. 3-hydroxyanthranilic acid inhibited the uptake of oxLDL by macrophages, an initiating event in the formation of foam cells, a major cellular component of atherosclerotic lesions. Surprisingly, 3-HAA significantly affected plasma cholesterol and triglyceride levels in Ldlr/ mice, likely due to modulation of signalling through peroxisome proliferator-activated receptors. 3-Hydroxyanthranilic acid inhibits atherosclerosis by regulating lipid metabolism and inflammation, two major components of this disease.
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