Abstract
The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor that binds diverse endogenous and xenobiotic ligands, which regulate AHR stability, transcriptional activity, and cell signaling. AHR activity is strongly implicated throughout the course of chronic kidney disease (CKD). Many diverse organic molecules bind and activate AHR and these ligands are reported to either promote glomerular and tubular damage or protect against kidney injury. AHR crosstalk with estrogen, peroxisome proliferator-activated receptor-γ, and NF-κB pathways may contribute to the diversity of AHR responses during the various forms and stages of CKD. The roles of AHR in kidney fibrosis, metabolism and the renin angiotensin system are described to offer insight into CKD pathogenesis and therapies.
Highlights
Chronic kidney disease (CKD) affects approximately 37 million (1 in 7) US adults and is the ninth leading cause of death (CDC, 2020)
This study further demonstrated that indoxyl sulfateexposed human kidney-2 (HK-2) proximal tubular cells reduced Mas receptor expression and this response was antagonized by Ang-(1–7) pre-treatment or by the absence of aryl hydrocarbon receptor (AHR) (Ng et al, 2014)
The elevated levels of uremic solutes that act as AHR ligands during the progression of chronic kidney disease (CKD) highlight the significance of AHR activity in these diseases
Summary
Chronic kidney disease (CKD) affects approximately 37 million (1 in 7) US adults and is the ninth leading cause of death (CDC, 2020). Intracellular signals downstream from the TGF-β1 receptor stimulate interstitial myofibroblast proliferation and secretion of collagen and additional ECM proteins (Panizo et al, 2021), promote anaerobic metabolism (Zhao et al, 2020), regulate immune cell differentiation (Sanjabi et al, 2017), and induce the expression of integrins (Curran and Keely, 2013) and the nuclear factor-kappa-B (NF-κB) subunit, p65 (Sun et al, 2015).
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