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Background: Sleep disorders have been associated with auditory dysfunction. However, the specific effects of sleep fragmentation (SF) on the peripheral auditory system and the underlying mechanisms remain unclear.
Methods: Data from the National Health and Nutrition Examination Survey (NHANES) were analyzed to examine the association between sleep disturbances and difficulties in speech perception in noisy environments among participants with normal audiograms. Additionally, an SF mouse model was used to assess the impact of sleep disruption on auditory function and cochlear pathology. Auditory brainstem response (ABR) testing, immunofluorescence staining, and transmission electron microscopy were performed to evaluate the auditory system.
Results: NHANES data revealed that individuals with sleep disorders, even with normal audiograms, were more likely to experience difficulties in speech perception in noisy environments. In the mouse model, chronic SF led to a significant decrease in the amplitude and a prolonged latency of ABR wave I, without detectable changes in hearing thresholds. Immunofluorescence staining revealed a significant decrease in the number of ribbon synapses in inner hair cells and an increase in orphan ribbons. Moreover, electron microscopy demonstrated myelin damage in the auditory nerve fibers.
Conclusions: Sleep fragmentation induces subtle damage to the auditory system, particularly affecting inner hair cell synapses and auditory nerve fibers, which may underlie difficulties in speech recognition in noisy environments, a potential indicator of hidden hearing loss.
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http://dx.doi.org/10.1002/brb3.70778 | DOI Listing |
JCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
View Article and Find Full Text PDFJCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDFJ Clin Invest
September 2025
Department of Cellular and Molecular Medicine, UCSD, La Jolla, United States of America.
3-O-sulfation of heparan sulfate (HS) is the key determinant for binding and activation of Antithrombin III (AT). This interaction is the basis of heparin treatment to prevent thrombotic events and excess coagulation. Antithrombin-binding HS (HSAT) is expressed in human tissues, but is thought to be expressed in the subendothelial space, mast cells, and follicular fluid.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
School of Medicine, Chongqing University, Chongqing 400044, China.
Engineering functional exosomes represents a cutting-edge approach in biomedicine, holding the promise to transform targeted therapy. However, challenges such as achieving consistent modification and scalability have limited their wider adoption. Herein, we introduce a universal and effective strategy for engineering multifunctional exosomes through cell fusion.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
State Key Laboratory of Bioactive Molecules and Druggability Assessment, Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine and New Drugs Research, International Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug De
Proliferative retinopathy is a leading cause of irreversible blindness in humans; however, the molecular mechanisms behind the immune cell-mediated retinal angiogenesis remain poorly elucidated. Here, using single-cell RNA sequencing in an oxygen-induced retinopathy (OIR) model, we identified an enrichment of sorting nexin (SNX)-related pathways, with SNX3, a member of the SNX family that is involved in endosomal sorting and trafficking, being significantly upregulated in the myeloid cell subpopulations of OIR retinas. Immunostaining showed that SNX3 expression is markedly increased in the retinal microglia/macrophages of mice with OIR, which is mainly located within and around the neovascular tufts.
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