| Autor: |
Jasmer KJ; Christopher S. Bond Life Sciences Center, Department of Biochemistry, The University of Missouri, Columbia, MO 65211-7310, USA., Gilman KE; Department of Nutritional Sciences, The University of Arizona, Tucson, AZ 85721, USA., Muñoz Forti K; Christopher S. Bond Life Sciences Center, Department of Biochemistry, The University of Missouri, Columbia, MO 65211-7310, USA., Weisman GA; Christopher S. Bond Life Sciences Center, Department of Biochemistry, The University of Missouri, Columbia, MO 65211-7310, USA., Limesand KH; Department of Nutritional Sciences, The University of Arizona, Tucson, AZ 85721, USA. |
| Abstrakt: |
Salivary glands sustain collateral damage following radiotherapy (RT) to treat cancers of the head and neck, leading to complications, including mucositis, xerostomia and hyposalivation. Despite salivary gland-sparing techniques and modified dosing strategies, long-term hypofunction remains a significant problem. Current therapeutic interventions provide temporary symptom relief, but do not address irreversible glandular damage. In this review, we summarize the current understanding of mechanisms involved in RT-induced hyposalivation and provide a framework for future mechanistic studies. One glaring gap in published studies investigating RT-induced mechanisms of salivary gland dysfunction concerns the effect of irradiation on adjacent non-irradiated tissue via paracrine, autocrine and direct cell-cell interactions, coined the bystander effect in other models of RT-induced damage. We hypothesize that purinergic receptor signaling involving P2 nucleotide receptors may play a key role in mediating the bystander effect. We also discuss promising new therapeutic approaches to prevent salivary gland damage due to RT. |
