ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Unraveling Endocannabinoid Signaling Pathways in Cisplatin-Induced Ototoxicity.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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
Cisplatin-induced ototoxicity is a detrimental side effect of chemotherapy leading to hearing loss, for which no treatments are currently available. Despite the growing recognition of the endocannabinoid (eCB) system (ECS) as a significant contributor to different physiological and pathological processes, its role in hearing remains poorly investigated. To fill this knowledge gap, we performed a molecular profiling of the ECS in auditory hair cell (HC)-like UB/OC1 cells derived from the mouse organ of Corti (OC), demonstrating the presence of the main eCBs-binding receptors and metabolic enzymes along with the major eCBs (N-arachidonoylethanolamine, AEA, and 2-arachidonoylglycerol, 2-AG) and additional eCB-like compounds. Subsequently, we established an in vitro model of cisplatin-induced ototoxicity, which was characterized by the downregulation of the HC marker myosin 7a (Myo 7a), and activation of nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) associated with caspase-3-mediated cell death. In this model, we observed a downregulation of cannabinoid receptor 2 (CB
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