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Crosstalk between Tryptophan Metabolism and Cardiovascular Disease, Mechanisms, and Therapeutic Implications
Gang Liu1, Shuai Chen1, Jin Zhong2
1Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, Hunan Provincial Engineering Research Center of Healthy Livestock, Scientific Observing and Experimental Station of Animal Nutrition and Feed Science in South-Central, Ministry of Agriculture, Hunan Co-Innovation Center of Animal Production Safety, Hunan 410125, China.
Insights
Inflammation in atherosclerosis impacts indoleamine 2,3-dioxygenase (IDO1). This enzyme
Area of Science:
- Immunology
- Biochemistry
- Cardiovascular Medicine
Background:
- Cardiovascular diseases (CVD), primarily coronary heart disease and stroke, stem from atherosclerosis.
- Atherosclerosis is a chronic inflammatory disease of the artery wall driven by maladaptive immune responses.
- Tryptophan (Trp) metabolism via the kynurenine (Kyn) pathway produces metabolites influencing inflammation.
Purpose of the Study:
- To review recent literature on the kynurenine pathway of tryptophan degradation in CVD.
- To highlight the role of indoleamine 2,3-dioxygenase (IDO1) in tryptophan metabolism within CVD.
Main Methods:
- Literature review of studies on kynurenine pathway and CVD.
- Focus on the function of IDO1-mediated tryptophan metabolism.
Main Results:
- Inflammation in early atherosclerosis affects IDO1 activity.
- IDO1 and its pathway are key mediators of immunoinflammatory responses in advanced atherosclerosis.
Conclusions:
- IDO1-mediated tryptophan metabolism is a critical factor in the immunoinflammation of atherosclerosis.
- Understanding this pathway offers insights into CVD pathogenesis.
Abstract:
The cardiovascular diseases (CVD) associated with the highest rates of morbidity are coronary heart disease and stroke, and the primary etiological factor leading to these conditions is atherosclerosis. This long-lasting inflammatory disease, characterized by how it affects the artery wall, results from maladaptive immune responses linked to the vessel wall. Tryptophan (Trp) is oxidized in a constitutive manner by tryptophan 2,3-dioxygenase in liver cells, and for alternative cell types, it is catalyzed in the presence of a differently inducible indoleamine 2,3-dioxygenase (IDO1) in the context of a specific pathophysiological environment. Resultantly, this leads to a rise in the production of kynurenine (Kyn) metabolites. Inflammation in the preliminary stages of atherosclerosis has a significant impact on IDO1, and IDO1 and the IDO1-associated pathway constitute critical mediating agents associated with the immunoinflammatory responses that characterize advanced atherosclerosis. The purpose of this review is to survey the recent literature addressing the kynurenine pathway of tryptophan degradation in CVD, and the author will direct attention to the function performed by IDO1-mediated tryptophan metabolism.