The immunometabolic role of indoleamine 2, 3-dioxygenase in atherosclerotic cardiovascular disease: immune homeostatic mechanisms in the artery wall. Issue 9 (7th March 2019)

• Record Type: Journal Article
• Authors: Ketelhuth, Daniel F J
• Is Part Of: Cardiovascular research. Volume 115:Issue 9(2019)
• Page Start: 1408
• Page End: 1415
• Publication Date: 2019-03-07
• Subjects: Atherosclerosis -- IDO -- Kynurenine -- Inflammation -- Immunometabolism; Cardiovascular system -- Diseases -- Periodicals; Cardiovascular system -- Periodicals; 616.1
• DOI: 10.1093/cvr/cvz067
• Languages: English
• ISSNs: 0008-6363

Abstract

Abstract: Coronary heart disease and stroke, the two most common cardiovascular diseases worldwide, are triggered by complications of atherosclerosis. Atherosclerotic plaques are initiated by a maladaptive immune response triggered by accumulation of lipids in the artery wall. Hence, disease is influenced by several non-modifiable and modifiable risk factors, including dyslipidaemia, hypertension, smoking, and diabetes. Indoleamine 2, 3-dioxygenase (IDO), the rate-limiting enzyme in the kynurenine pathway of tryptophan (Trp) degradation, is modulated by inflammation and regarded as a key molecule driving immunotolerance and immunosuppressive mechanisms. A large body of evidence indicates that IDO-mediated Trp metabolism is involved directly or indirectly in atherogenesis. This review summarizes evidence from basic and clinical research showing that IDO is a major regulatory enzyme involved in the maintenance of immunohomeostasis in the vascular wall, as well as current knowledge about promising targets for the development of new anti-atherosclerotic drugs. Graphical Abstract: