NADPH oxidase 3 inhibition preserves hearing in mice after stereotactic radiosurgery.
Overview
- The Inner Ear and Olfaction Lab, University of Geneva, Faculty of Medicine, 1211 Geneva, Switzerland
- Service of Otorhinolaryngology-Head and Neck Surgery, Department of Clinical Neurosciences, Geneva University Hospitals, 1205 Geneva, Switzerland
- Signal Processing Laboratory 5, École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland
- Department of Radiology, Lausanne University Hospital (CHUV), 1011 Lausanne, Switzerland
- Neurosurgery Service and Gamma Knife Center, Lausanne University Hospital (CHUV), Rue du Bugnon 44-46, BH-08, 1011 Lausanne, Switzerland
- Hôpital de La Tour, Centre NeuroKnife, Av. J.-D.-Maillard 3, 1217 Meyrin, Switzerland
Abstract
Stereotactic radiosurgery (SRS) is a standard treatment for vestibular schwannoma but is associated with a substantial risk of progressive and irreversible hearing loss. NADPH oxidase 3 (NOX3), an enzyme predominantly expressed in the inner ear, has been identified as a key source of oxidative stress underlying cochlear injury. Using a mouse model of SRS-induced hearing loss, we found that genetic deletion of Nox3 preserved auditory function and protected cochlear structures, including hair cells, synaptic ribbons, and spiral ganglion neurons. Complementary experiments using local delivery of a small interfering RNA directed against Nox3 confirmed that transient inhibition markedly reduced hearing loss and tissue damage compared with scrambled controls. In addition, Nox3 inhibition attenuated radiation-induced lipid peroxidation and macrophage infiltration within the cochlea. These findings identify NOX3-derived oxidative stress as an important upstream mediator of SRS-induced ototoxicity and demonstrate that its inhibition confers significant functional and structural protection. Given the predictable timing of SRS in clinical settings, a NOX3-targeted intervention may offer a feasible and selective strategy to prevent hearing loss as an adjunct to tumor-directed treatment.
Reproduced under the paper's license (CC BY), from the paper cited above.
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The data supporting the findings of this study are available from the corresponding author upon reasonable request.
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Version 2, 28 September 2026
- Authors: added Dimitrios Daskalou (0000-0003-3618-9776); Jean-Philippe Thiran (0000-0003-2938-9657); Constantin Tuleasca (0000-0001-6776-1486); removed Dimitrios Daskalou; Jean-Philippe Thiran; Constantin Tuleasca
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 9 authors, 10 keywords, 2 funders, 78 references.
Cite
This paper
Daskalou, D., Rousset, F., Sgroi, S., Oberhauser, L., Thiran, J.-P., Tuleasca, C., Jelescu, I. O., Levivier, M., & Senn, P. (2026). NADPH oxidase 3 inhibition preserves hearing in mice after stereotactic radiosurgery. Molecular therapy. Nucleic acids, 37(3), 103036. https://
BibTeX
@article{daskalou2026nad
author = {Daskalou, Dimitrios and Rousset, Francis and Sgroi, Stéphanie and Oberhauser, Lucie and Thiran, Jean-Philippe and Tuleasca, Constantin and Jelescu, Ileana O. and Levivier, Marc and Senn, Pascal},
title = {{NADPH oxidase 3 inhibition preserves hearing in mice after stereotactic radiosurgery}},
journal = {Molecular therapy. Nucleic acids},
year = {2026},
month = jul,
volume = {37},
number = {3},
pages = {103036},
publisher = {American Society of Gene \& Cell Therapy},
issn = {2162-2531},
doi = {10.1016/
url = {https://
pmid = {42621021},
pmcid = {PMC13487719}
}
RIS
TY - JOUR
AU - Daskalou, Dimitrios
AU - Rousset, Francis
AU - Sgroi, Stéphanie
AU - Oberhauser, Lucie
AU - Thiran, Jean-Philippe
AU - Tuleasca, Constantin
AU - Jelescu, Ileana O.
AU - Levivier, Marc
AU - Senn, Pascal
TI - NADPH oxidase 3 inhibition preserves hearing in mice after stereotactic radiosurgery
T2 - Molecular therapy. Nucleic acids
J2 - Mol Ther Nucleic Acids
PY - 2026
DA - 2026/
VL - 37
IS - 3
SP - 103036
SN - 2162-2531
PB - American Society of Gene & Cell Therapy
DO - 10.1016/
UR - https://
LA - en
ER -
CSL-JSON
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