ArticleJournal of translational medicine2026
CB2R agonism protects intestinal epithelium through β-catenin/HoxA10 loop in radiation injury.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundRadiation-induced intestinal injury (RIII) represents a significant dose-limiting complication of radiotherapy, characterized by substantial loss of intestinal epithelial cells (IECs). While the activation of cannabinoid receptor 2 (CB2R) is protective in immune‑mediated colitis, the intrinsic role of CB2R in IECs and its potential therapeutic relevance in RIII have not been defined.
methodsAn RIII mouse model was established in wild-type and CB2R
resultsIrradiation induced CB2R expression in the intestinal epithelium, and genetic ablation of CB2R markedly aggravated RIII. A focused pharmacological screen identified a recently synthesized dual‑target compound, CB2R/FAAH modulator‑2 (CF‑2), which combines CB2R agonistic activity with fatty acid amide hydrolase (FAAH) inhibition and significantly mitigated radiation‑induced colonic injury while exerting protective effects on the small intestine and spleen. Mechanistically, CB2R activation attenuated irradiation‑induced ferroptosis and preserved intestinal epithelial integrity. Integrative transcriptomic analyses identified Homeobox A10 (HoxA10) as a critical epithelial‑enriched transcriptional amplifier that reinforced CB2R/β‑catenin signaling through a positive‑feedback loop, thereby enhancing CB2R‑mediated epithelial protection.
conclusionsThis study defines an epithelial‑intrinsic CB2R signaling axis in RIII, linking ferroptosis suppression to preservation of intestinal barrier integrity. CF‑2 is positioned as a promising mechanism‑based candidate for radioprotection.
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