Despite decades of intense research physiologic aryl hydrocarbon receptor (AHR) functions have not been elucidated. Challenges include marked species differences and dependence on cell type and cellular context. A previous commentary on human AHR functions in skin and intestine has been extended to vascular tissue. Similar functions appear to be operating in vascular tissue including microbial defense, modulation of stem/progenitor cells as well as control of immunity and inflammation. However, AHR functions are Janus faced: Detrimental AHR functions in vascular tissue are well documented, e.g., upon exposure to polycyclic aromatic hydrocarbons in cigarette smoke leading to oxidative stress and generation of oxidized LDL. Modified LDL particles accumulate in macrophages and smooth muscle-derived pro-inflammatory foam cells, the hallmark of atherosclerosis. On the other hand, numerous anti-inflammatory AHR agonists have been identified including bilirubin and quercetin. Mechanisms as to how AHR produces pro- and anti-inflammatory responses in the vascular system need further investigation.
Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin = TCDD (PubChem CID: 15625); 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester) = ITE (PubChem CID: 4668801); 6-Formylindolo[3,2-b]carbazole = FICZ (PubChem CID: 3071); AHR functions; Baicalin (PubChem CID: 71311447); Bilirubin; Bilirubin (PubChem CID: 5280352); Indoxyl sulfate (PubChem CID: 10258); Kynurenine (PubChem CID: 846); OxLDL; Quercetin; Quercetin (PubChem CID: 5280343); Vascular tissue.
Copyright © 2018. Published by Elsevier Inc.