Table 2 The impact of AhR activation on kidney diseases and complications

CKD

Human aortic vascular smooth muscle cell

Accelerate thrombosis

AhR stabilized TF expression by inhibiting TF ubiquitination and degradation.

[41]

HUVEC and PBMC

Accelerate atherogenesis

AhR increased TF expression.

[42]

HUVEC

Accelerate thrombosis

Increased TF expression was regulated by AhR/p38 MAPK/NF-κB pathway.

[93]

HUVEC

N/A

AhR promoted neuronal pentraxin 1 transcription.

[94]

Human dermal microvascular endothelial cell

Suppress postischemic angiogenesis and promote PAD

AhR augmented β-catenin ubiquitination and degradation and then suppressed Wnt/β-catenin signaling pathway.

[98]

Skeletal muscle cell

Exacerbate the ischemic myopathy and PAD

N/A

[99]

HUVEC

Exacerbate vascular inflammation

AhR stimulated the transcriptional activity of activator protein 1 and then upregulated E-selectin expression, leading to the aggravation of leukocyte recruitment to the vascular wall.

[101]

Macrophage

Promote inflammation

AhR increased the transcription of Socs2 and Tnf-α.

[102]

N/A

Promote blood–brain barrier disruption associated with cognitive impairment

N/A

[87]

Astrocyte

Induce anxiety, cognitive impairment, astrocyte reactivation and neuronal activity enhancement

AhR downregulated GLT1 expression and activity and promoted pro-oxidant NOX1 expression.

[44]

RTEC

Enhance IS clearance

Elevated IS levels induced robust increases in the expression and transport activity of OAT1 by activating the AhR/ARNT and EGFR pathways.

[40]

Hepatocyte

Increase hepatic cyclosporine clearance

AhR upregulated P-glycoprotein expression and activity.

[43]

DN

MC and RTEC

Promote MC activation and extracellular matrix production

AhR was bound to the promoters of Cox-2, fibronectin, and collagen IV.

[122]

AKI

RTEC

Inhibit renal inflammation, pathological injury and apoptosis

AhR inhibited NF-κB and JNK pathways.

[128]

RTEC

Promote tubular cell survival against cisplatin toxicity and protect the kidney from cisplatin-induced acute injury

Elevated miR-125b transcriptionally by Nrf2 inhibited AhRR, increasing the transcriptional activity of AhR, promoting MDM2 expression, and then inhibiting p53 activity.

[130]

N/A

Limit renal damage during malaria

N/A

[131]

RTEC

Promote apoptosis and renal damage

AhR induced oxidative stress by increasing ROS.

[132]

RTEC

Accelerate cellular senescence, kidney dysfunction and tubular injury

AhR upregulated EZH2 expression, and EZH2 conversely enhanced AhR expression via weakening H3K27me3 transcriptional inhibition on the AhR promoter.

[133]

RTEC

Do not affect cellular senescence

N/A

[134]

OSA

N/A

Promote the progression of HTN induced by CIH

AhR antagonist CH223191 prevented the increase in systolic blood pressure by 53 ± 12% and diastolic blood pressure by 44 ± 16%.

[136]