Deficiency of the aryl hydrocarbon receptor in kidney epithelial cells does not influence the development of atherosclerosis.
R, H., C, R., K, A., M, R., C, S., & EPC, v.d.V. (2026). Deficiency of the aryl hydrocarbon receptor in kidney epithelial cells does not influence the development of atherosclerosis.. Scientific reports. https://doi.org/10.1038/s41598-026-63808-1
R H, C R, K A, M R, C S, EPC vdV. Deficiency of the aryl hydrocarbon receptor in kidney epithelial cells does not influence the development of atherosclerosis.. Scientific reports. 2026; doi: 10.1038/s41598-026-63808-1
R H, C R, K A, et al. Deficiency of the aryl hydrocarbon receptor in kidney epithelial cells does not influence the development of atherosclerosis.[J]. Scientific reports. 2026. DOI: 10.1038/s41598-026-63808-1.
@article{r2026,
author = {Huchzermeier R and Romel C and Abschlag K and Rogg M and Schell C and van der Vorst EPC},
title = {Deficiency of the aryl hydrocarbon receptor in kidney epithelial cells does not influence the development of atherosclerosis.},
journal = {Scientific reports},
year = {2026},
doi = {10.1038/s41598-026-63808-1},
note = {PMID: 42521707},
}
TY - JOUR AU - Huchzermeier R AU - Romel C AU - Abschlag K AU - Rogg M AU - Schell C AU - van der Vorst EPC TI - Deficiency of the aryl hydrocarbon receptor in kidney epithelial cells does not influence the development of atherosclerosis. T2 - Scientific reports PY - 2026 DO - 10.1038/s41598-026-63808-1 AN - PMID:42521707 ER -
The aryl hydrocarbon receptor (AHR) is recognised as an important mediator of inflammatory processes, including those in kidney health. Patients suffering from kidney diseases have an increased risk of cardiovascular diseases, such as atherosclerosis. Since the AHR can be activated in the kidney by, e.g., tryptophan metabolites and contribute to inflammatory processes, we hypothesized that a deficiency of the Ahr in the kidney epithelium in mice fed a high-fat diet could impact the development of atherosclerosis by altering renal function. We analysed Apoe-/-Cdh16CreAhrfl/fl mice in comparison to Apoe-/-Ahrfl/fl after feeding a 12-week high-fat diet in terms of systemic inflammation, plaque, and kidney phenotype. Accordingly, we found that the absence of Ahr in the kidney epithelium did not affect atherosclerotic outcomes and, surprisingly, did not alter the kidney phenotype with respect to inflammation or fibrosis. We therefore concluded that a high-fat diet does not sufficiently drive an AHR-mediated response in kidney epithelium, which could contribute to plaque development.