Cytomegalovirus (CMV) represents the most prevalent cause of congenital viral infection in newborns and the leading non-genetic etiology of sensorineural hearing loss (SNHL) in children. Notably, only 10–15% of congenitally infected infants possibly present with classic clinical symptoms at birth, including Small for gestational age, Microcephaly, Petechiae or purpura, Blueberry muffin rash, Jaundice, Hepatomegaly, Splenomegaly and abnormal neurologic signs. In contrast, approximately 90% of infected neonates exhibit no apparent symptoms initially. Current research predominantly focuses on symptomatic cases due to their severe acute presentations and high rates of long-term sequelae (40–60%), including SNHL and neurodevelopmental impairments. However, significant controversy persists regarding the management of asymptomatic infants. Emerging evidence reveals that 8–15% of asymptomatic carriers develop Late-onset Hearing Loss (LOHL) beyond the neonatal period. Additionally, 5–10% may manifest neurodevelopmental abnormalities including mild intellectual disability, learning difficulties, or motor coordination disorders. Crucially, given the substantial population of asymptomatic cCMV cases, these delayed complications account for 30–40% of all cCMV-related long-term morbidity, underscoring their considerable public health impact. This review synthesizes current evidence and controversies regarding cCMV-related SNHL in asymptomatic or mildly symptomatic children, with a focus on screening, diagnostic classification, and antiviral management gaps, to heighten clinical awareness of this underrecognized cause of hearing loss.

The calcium- and integrin-binding protein (CIB) family, comprising four evolutionarily conserved members (CIB1, CIB2, CIB3, and CIB4), is characterized by canonical EF-hand motifs. The functions of CIBs in the inner ear have been investigated, although further research is still necessary to gain a comprehensive understanding of them. Among the CIB family members, CIB2 is essential for auditory function. CIB3 and CIB2 jointly participate in the regulation of balance. Beyond their sensory roles, CIBs exhibit multifunctionality through calcium-dependent interactions with diverse molecular partners, contributing to the pathogenesis of various conditions, including neurological disorders, cardiovascular diseases, cancer, and male infertility. In this review, we discuss the conserved structure of the CIB family, highlighting its contributions to various biological functions. We also summarize the distribution and function of the CIB family, emphasizing the pivotal roles of CIB2 and CIB3 in hearing and balance.

Objectives: Observational studies have shown that chronic obstructive pulmonary disease (COPD) is associated with an increased risk of hearing impairment. However, causality remains unclear, including with respect to lung function. This study aimed to investigate the associations of lung function and COPD with hearing impairment in the UK Biobank and confirm potential causalities using Mendelian randomization (MR). Methods: Cross-sectional analyses were performed using logistic regression models in a subsample of the UK Biobank. Two-sample MR analyses were performed on summary statistics for forced expiratory volume in one second (FEV1), forced vital capacity (FVC), COPD, and sensorineural hearing loss. Results: FEV1 and FVC were negatively associated with hearing impairment, with odds ratios (95% confidence intervals) of 0.80 (0.77, 0.84) and 0.80 (0.76, 0.83), respectively. COPD was positively associated with hearing impairment, with an odds ratio (95% confidence interval) of 1.10 (1.02, 1.18). In the MR analyses, a negative association was found between FVC and sensorineural hearing loss, with an odds ratio (95% confidence interval) of 0.91 (0.83, 0.99). For FVE1 and COPD, no significant associations were found. Conclusions: The results of this study showed that FVC was causally associated with hearing impairment, suggesting a potential protective effect of FVC on hearing impairment.

Cytomegalovirus (CMV) represents the most prevalent cause of congenital viral infection in newborns and the leading non-genetic etiology of sensorineural hearing loss (SNHL) in children. Notably, only 10%-15% of congenitally infected infants possibly present with classic clinical symptoms at birth, including Small for gestational age, Microcephaly, Petechiae or purpura, Blueberry muffin rash, Jaundice, Hepatomegaly, Splenomegaly and abnormal neurologic signs. In contrast, approximately 90% of infected neonates exhibit no apparent symptoms initially. Current research predominantly focuses on symptomatic cases due to their severe acute presentations and high rates of long-term sequelae (40%-60%), including SNHL and neurodevelopmental impairments. However, significant controversy persists regarding the management of asymptomatic infants. Emerging evidence reveals that 8%-15% of asymptomatic carriers develop Late-onset Hearing Loss (LOHL) beyond the neonatal period.Additionally 5%-10% may manifest neurodevelopmental abnormalities including mild intellectual disability, learning difficulties, or motor coordination disorders. Crucially, given the substantial population of asymptomatic cCMV cases, these delayed complications account for 30%-40% of all cCMV-related long-term morbidity, underscoring their considerable public health impact. This review synthesizes current evidence and controversies regarding cCMV-related SNHL in asymptomatic or mildly symptomatic children, with a focus on screening, di-agnostic classification, and antiviral management gaps, to heighten clinical awareness of this underrecognized cause of hearing loss.

Tinnitus is a prevalent and distressing medical symptom, and no effective pharmacological treatment currently exists. Despite significant advances, tinnitus remains a scientific enigma. To explore the molecular underpinnings of tinnitus, we developed a noise-induced tinnitus model in mice and utilized metabolomics to identify key differences in metabolic pathways. Our results revealed that oxidative stress-related pathways, including glutathione (GSH) metabolism, were significantly enriched in the auditory cortex of mice exhibiting tinnitus-like behavior. To further explore the role of oxidative stress, we examined the involvement of nuclear factor erythroid 2-related factor 2 (Nrf2) in tinnitus by conducting experiments in Nrf2 knockout (Nrf2-KO) mice. While Nrf2-deficient mice did not develop spontaneous tinnitus or hearing loss, they displayed increased susceptibility to prolonged tinnitus-like behavior after noise exposure. This was accompanied by heightened microglial activation, neuroinflammation, and significant alterations in gut microbiota composition, including greater diversity and dysbiosis. Our findings highlight a novel mechanism underlying tinnitus, emphasizing the role of oxidative stress in the auditory cortex and its connection to noise-induced tinnitus. The deficiency of Nrf2 in mice increases their susceptibility to tinnitus, suggesting that Nrf2 may serve as a promising therapeutic target for preventing noise-induced tinnitus.

Rationale: Semicircular canal occlusion (SCO) is used to treat vestibular vertigo with demonstrated efficacy. This study introduces a novel transcanal endoscopic approach for horizontal SCO to manage vertigo in refractory Meniere’s disease (MD). Patient concerns: Four patients with refractory MD, previously managed conservatively for over 6 months, presented with severe-to-profound hearing loss. Their vertigo symptoms progressively worsened and severely compromised quality of life. Diagnoses: All 4 patients met diagnostic criteria for definite MD with severe-to-profound hearing loss. Interventions: All patients underwent transcanal endoscopic horizontal SCO with a 12-month postoperative follow-up to evaluate clinical outcomes and procedural safety. Outcomes: Postoperative vertigo control was effective, demonstrating significant reductions in both attack frequency and symptom intensity. Subjective tinnitus improved in 1 patient and remained stable in the remaining 3. Hearing thresholds were preserved in all cases without progression. Transient postoperative disequilibrium occurred in 1 patient, resolving spontaneously without complications. Lessons: Transcanal endoscopic horizontal SCO represents a safe, effective, and clinically viable alternative to pharmacologic conservative management for refractory MD with severe-to-profound hearing loss persisting beyond 6 months.