Aryl hydrocarbon receptor (AHR)
AHR (aryl hydrocarbon receptor) is a ligand-activated transcription factor best known for sensing a wide range of endogenous Metabolites and environmental compounds.
AHR (aryl hydrocarbon receptor) is a ligand-activated transcription factor best known for sensing a wide range of endogenous Metabolites and environmental compounds. In biomedical research, it is commonly studied as a regulator of immune signaling, epithelial barrier function, xenobiotic response, and metabolic adaptation. Upon activation by agonists such as indole-derived microbial Metabolites or therapeutic small molecules, AHR can influence downstream pathways including NF-κB, MAPK, NLRP3-related inflammatory signaling, and lipid metabolism.
Recent studies have highlighted AHR as a mechanistic node linking the gut microbiota, mucosal integrity, inflammatory control, and tissue repair. In the contexts provided here, AHR was investigated in intestinal disease, skin inflammation, spinal cord injury, and cancer-related metabolic remodeling, often in combination with compounds such as tapinarof, indole-3-propionic acid, indole-3-carbinol, and irinotecan-associated nanomedicine strategies. These studies collectively support AHR as a biologically important target in inflammation-associated and metabolism-associated disease processes.
Rebuilt from PubMed 10 Sept 2026 · no new papers today
Where the papers sit
8 papers study aryl hydrocarbon receptor (ahr) directly. Those 8 do not group into themes. AHR recurs as a link between microbial, dietary and metabolic signals and tissue barriers, inflammation, fibrosis and cancer. The studies do not converge on a shared disease question or therapeutic direction. They are no more alike than papers drawn from anywhere in the corpus.
Recent Findings on Aryl hydrocarbon receptor (AHR) — latest 30 papers
Recent studies positioned Aryl hydrocarbon receptor (AHR) as a mechanistic node linking tryptophan-derived Metabolites, inflammation, and tissue injury across metabolic, intestinal, dermatologic, oncologic, and neurologic models. In a mouse model of diet-induced and genetic insulin resistance, 5-methoxytryptamine improved hepatic inflammation, insulin resistance, and steatosis, and the beneficial metabolic effects were attenuated by specific AHR inhibition, indicating AHR dependence 42365576Jun. In parallel, food-grade TiO2–induced intestinal injury was associated with gut microbiota dysbiosis and reduced Lactobacillus-derived indole-3-lactic acid, described as an AHR agonist, in the context of impaired mucin sulfation and mucosal barrier damage 42289709Jun.
AHR was also leveraged therapeutically in cancer and inflammatory skin disease. In colorectal cancer models, indole-3-carbinol was used as an AHR agonist in a self-assembled irinotecan nanomedicine, where activation of the AHR/CPT1A axis promoted fatty acid oxidation in hepatocytes and abolished irinotecan-driven steatohepatitis-associated liver metastasis while also enhancing antitumor efficacy 42007878Apr. In psoriasis-related in vitro work, tapinarof, a novel AHR agonist, was evaluated in nanogel form in an imiquimod-induced HaCaT-THP-1 co-culture model, where it showed stronger anti-inflammatory, anti-proliferative, and anti-migratory effects than free tapinarof, with reduced cytokine-associated inflammatory responses 41864521Mar.
In neuroinflammation, indole-3-propionic acid (IPA) was shown to act through AHR to suppress astrocyte activation after spinal cord injury. Using TNF-α-stimulated astrocytes and a mouse SCI model, IPA reduced pro-inflammatory mediators including IL-6, IL-1β, iNOS, COX-2, CCL2, CXCL2, and CXCL10, and mechanistic analyses indicated inhibition of NF-κB/MAPK signaling via AHR activation 41663028Feb. These effects were accompanied by reduced glial scar formation, improved neuronal survival, and better long-term motor recovery in vivo 41663028Feb.
Written from 8 PubMed abstracts, each one cited by PMID above. Published: 2026-06-16. Last written: 2026-07-29 by GPT. Drafted by language models from published abstracts; not medical advice.