ArticleJournal of molecular histology2026
Anti-LCN2 antibody treatment is associated with attenuated hearing loss and blood-labyrinth barrier disruption in a mouse model of chronic kidney disease.
Article in Journal of molecular histology, 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
Chronic kidney disease (CKD) is associated with sensorineural hearing loss, but the mechanisms linking renal injury to cochlear dysfunction remain incompletely defined. Because lipocalin-2 (LCN2/NGAL) is markedly increased in CKD and has been implicated in endothelial dysfunction and barrier injury, we investigated whether LCN2 contributes to cochlear damage in a mouse model of CKD. Male C57BL/6J mice underwent 5/6 nephrectomy, and CKD mice received either an anti-LCN2 monoclonal antibody or an isotype control three times weekly for seven weeks beginning one week after completion of surgery. Auditory function, cochlear morphology, blood-labyrinth barrier integrity, cochlear perfusion, and LCN2-associated signaling were assessed using auditory brainstem responses, distortion product otoacoustic emissions, whole-mount immunofluorescence, FITC-dextran extravasation, Western blotting, quantitative PCR, and laser Doppler flowmetry. CKD mice developed elevated auditory brainstem response thresholds, reduced distortion product otoacoustic emission amplitude at a single primary tone pair with f2 = 8.0 kHz, outer hair cell loss, and a reduction in the number of CtBP2-positive presynaptic ribbon puncta per inner hair cell. These changes were accompanied by increased serum and cochlear LCN2, upregulation of 24p3R/SLC22A17 and NLRP3, increased blood-labyrinth barrier permeability, reduced claudin-5 and ZO-1 expression, impaired cochlear blood flow, stria vascularis atrophy, and decreased expression of strial ion-transport genes. Anti-LCN2 antibody treatment improved auditory thresholds and otoacoustic emission responses, attenuated outer hair cell and synaptic injury, reduced vascular leakage, partially restored tight junction and ion-transport gene expression, and improved cochlear perfusion, without measurably lowering serum blood urea nitrogen or creatinine. These findings support a possible contribution of LCN2 to CKD-associated cochlear vascular dysfunction and hearing loss. Targeting LCN2 may represent a therapeutic strategy for preserving hearing in CKD, although validation in additional CKD models, both sexes, and human tissues is required.
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