The role of aryl hydrocarbon receptor signalling in COVID-19 pathology and its therapeutic potential.

Frontiers in molecular medicine Pub Date : 2025-08-29 eCollection Date: 2025-01-01 DOI:10.3389/fmmed.2025.1599785
Saidon Mbambara, Ndimo Modipane, Thato Serite, Mike Sathekge, Mankgopo Kgatle
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Abstract

Coronavirus disease 2019 (COVID-19), caused by the betacoronavirus SARS-CoV-2, emerged in Wuhan, China, and rapidly evolved into a global health crisis. Recent evidence highlights the activation of the aryl hydrocarbon receptor (AHR) pathway following SARS-CoV-2 infection, implicating AHR in facilitating viral replication and impairing antiviral immunity. As a ligand-dependent transcription factor, AHR regulates immune responses, cellular differentiation, and proliferation, and is frequently exploited by viruses to evade host defences. In relation to COVID-19, AHR activation drives immune suppression, systemic inflammation, and metabolic disturbances, intensifying disease severity. Notably, in individuals with comorbidities such as obesity and diabetes, AHR overactivity exacerbates insulin resistance, oxidative stress, endothelial dysfunction, and thrombotic risk, contributing to cardiovascular complications. AHR also promotes airway remodelling and mucus hypersecretion, fostering respiratory dysfunction and fibrotic progression. This review synthesizes current insights into the mechanistic role of AHR signalling in SARS-CoV-2 pathogenesis and discusses its potential as a target for host-directed therapeutic interventions.

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芳烃受体信号在COVID-19病理中的作用及其治疗潜力
由冠状病毒SARS-CoV-2引起的2019冠状病毒病(COVID-19)在中国武汉出现,并迅速演变为全球卫生危机。最近的证据强调了在SARS-CoV-2感染后芳烃受体(AHR)途径的激活,暗示AHR促进病毒复制并损害抗病毒免疫。作为一种依赖配体的转录因子,AHR调节免疫反应、细胞分化和增殖,并经常被病毒利用来逃避宿主的防御。与COVID-19相关,AHR激活会导致免疫抑制、全身性炎症和代谢紊乱,从而加剧疾病的严重程度。值得注意的是,在患有肥胖和糖尿病等合并症的个体中,AHR过度活跃会加剧胰岛素抵抗、氧化应激、内皮功能障碍和血栓形成风险,从而导致心血管并发症。AHR还促进气道重塑和粘液分泌过多,促进呼吸功能障碍和纤维化进展。本综述综合了目前对AHR信号在SARS-CoV-2发病机制中的机制作用的见解,并讨论了其作为宿主导向治疗干预靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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