Abstract
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor originally isolated and characterized as the dioxin or xenobiotic receptor. With the discovery of endogenous ligands and studies of AhR knockout mice, AhR has been found to serve an important role in several biological processes, including immune responses and developmental and pathological regulation. In particular, it has been considered as a new major player in cardiovascular diseases. Recent studies have revealed that the development of atherosclerosis is closely associated with AhR function. However, the roles of the AhR in the pathological development of atherosclerosis and atherosclerosis-associated diseases remain unclear. The current review presents the molecular mechanisms involved in the regulation of AhR expression during inflammation, oxidative stress and lipid deposition. Additionally, the role of the AhR in atherosclerosis and atherosclerosis-associated diseases is reviewed.
Highlights
The aryl hydrocarbon receptor (AhR) is a ligand‐activated transcription factor originally isolated and characterized as the dioxin or xenobiotic receptor
These findings suggest that blood lipid parameters in patients with coronary angiography are significantly associated with GSTM1/T1/P1 genotype distribution and GSTT1 deletion polymorphisms
AhR expression and polymorphisms are associated with the risk of ischemic stroke
Summary
Atherosclerosis is a chronic inflammatory disease [27,28]. The pathology of atherosclerosis can be summarized as follows. The inflammatory factors induce the chemotaxis of monocytes in blood vessels into the stromal cells, where they differentiate into macrophages [32,33] This is the early development of atherosclerosis [34]. It has been validated by recent studies that the AhR detoxifies, and regulates lipid metabolism in the liver [51] Environmental pollutants such as TCDD and benzo(a)pyrene (BP) inhibit the expression of NPC intracellular cholesterol transporter 1 in an AhR‐dependent manner, promoting lipid deposition [52]. Activation of AhR protects against fatty liver induced by insulin resistance by activating fibroblast growth factor 21 (FGF21) to regulate lipid and energy metabolism in such mice [57]. PCB 153, mediated by AhR, can be considered as a ‘secondary strike’ mechanism for obesity/non‐alcoholic fatty liver disease in the context of a HFD [59]
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