Aminoglycosides, a class of clinically important drugs, are widely used worldwide against gram-negative bacterial infections. However, there is growing evidence that aminoglycosides can cause hearing loss or balance problems. In this article, we mainly introduce the main mechanism of ototoxicity induced by aminoglycosides. Genetic analysis showed that the susceptibility of aminoglycosides was attributable to mutations in mtDNA, especially A1555G and C1494T mutations in 12S rRNA. In addition, the overexpression of NMDA receptors and the formation of free radicals also play an important role. Understanding the mechanism of ototoxicity induced by aminoglycosides is helpful to develop new therapeutic methods to protect hearing. In this article, the prevention methods of ototoxicity induced by aminoglycosides were introduced from the upstream and downstream aspects.

Age-related hearing loss, or presbycusis, is a common cause of hearing loss in elderly people worldwide. It typically presents as progressive, irreversible, and usually affects the high frequencies of hearing, with a tremendous impact on the quality of life. Presbycusis is a complex multidimensional disorder, in addition to aging, multiple factors including exposure to noise, or ototoxic agents, genetic susceptibility, metabolic diseases and lifestyle can influence the onset and severity of presbycusis. With the aging of the body, its ability to clean up deleterious substances produced in the metabolic process is weakened, and the self-protection and repair function of the body is reduced, which in turn leads to irreversible damage to the cochlear tissue, resulting in the occurrence of presbycusis. Presently, oxidative stress (OS), mitochondrial DNA damage, low-grade inflammation, decreased immune function and stem cell depletion have been demonstrated to play a critical role in developing presbycusis. The purpose of this review is to illuminate the various mechanisms underlying this age-related hearing loss, with the goal of advancing our understanding, prevention, and treatment of presbycusis.

To investigate if the anxiety associated with coronavirus disease 2019 (COVID-19) is a promoting factor to tinnitus. A retrospective research design collected from 188 tinnitus patients, was used to compare the clinical characteristics of tinnitus between the patients in 2020 under pandemic pressure and those from the matching period in 2019. While anxiety was quantified using the Zung’s Self-rating Anxiety Scale (SAS), tinnitus severity was evaluated using the Tinnitus Handicap Inventory (THI) questionnaire and the test of tinnitus loudness (TL). The assessments were repeated after the sound therapy plus educational counselling (STEC) for 38 patients in 2020 and 58 patients in 2019 and compared with EC alone therapy for 42 patients in 2020 and 17 patients in 2019. A large increase in anxiety was evident in 2020 in both case rate and SAS. The treatment of both methods was less effective in 2020. SAS, THI and TL were all deteriorated after the EC alone treatment in 2020, while an improvement was seen in 2019. This suggests that EC alone could not counteract the stress by COVID-19 at all, and the stress, if not managed well, can significantly increase the severity of tinnitus and associated anxiety. By using the EC subgroup in virtual control, we conclude that anxiety can serve as a promoting factor to tinnitus. We believe that this is the first study report that confirm the causative/promotive role of anxiety on tinnitus during COVID-19 pandemic.

Background: The coronavirus disease 2019 (COVID-19) pandemic has spread worldwide. However, the impact of baseline lipid profile on clinical endpoints in COVID-19 and the potential effect of COVID-19 on lipid profile remain unclear.Methods: In this retrospective cohort study, we consecutively enrolled 430 adult COVID-19 patients from two Chinese hospitals (one each in Chengdu and Wuhan). The lipid profile before admission and during the disease course and the clinical endpoint including in-hospital death or oropharyngeal swab test positive again (OSTPA) after discharge were collected. We used Kaplan–Meier and Cox regression to explore the lipid risk factors before admission associated with endpoints. Then, we assessed the lipid level change along with the disease course to determine the relationship between pathology alteration and the lipid change.Results: In the Chengdu cohort, multivariable Cox regression showed that low-density lipoprotein cholesterol (LDL-C) dyslipidemia before admission was associated with OSTPA after discharge for COVID-19 patients (RR: 2.51, 95% CI: 1.19, 5.29, p = 0.006). In the Wuhan cohort, the patients with triglyceride (TG) dyslipidemia had an increased risk of in-hospital death (RR: 1.92, 95% CI: 1.08, 3.60, p = 0.016). In addition, in both cohorts, the lipid levels gradually decreased in the in-hospital death or OSTPA subgroups since admission. On admission, we also noticed the relationship between the biomarkers of inflammation and the organ function measures and this lipid level in both cohorts. For example, after adjusting for age, sex, comorbidities, smoking, and drinking status, the C-reactive protein level was negatively associated with the TC lipid level [β (SE) = -0.646 (0.219), p = 0.005]. However, an increased level of alanine aminotransferase, which indicates impaired hepatic function, was positively associated with total cholesterol (TC) lipid levels in the Chengdu cohort [β (SE) = 0.633 (0.229), p = 0.007].Conclusions: The baseline dyslipidemia should be considered as a risk factor for poor prognosis of COVID-19. However, lipid levels may be altered during the COVID-19 course, since lipidology may be distinctly affected by both inflammation and organic damage for SARS-CoV-2.

The prevalence of hearing loss-related diseases caused by different factors is increasing worldwide year by year. Currently, however, the patient’s hearing loss has not been effectively improved. Therefore, there is an urgent need to adopt new treatment measures and treatment techniques to help improve the therapeutic effect of hearing loss. G protein-coupled receptors (GPCRs), as crucial cell surface receptors, can widely participate in different physiological and pathological processes, particularly play an essential role in many disease occurrences and be served as promising therapeutic targets. However, no specific drugs on the market have been found to target the GPCRs of the cochlea. Interestingly, many recent studies have demonstrated that GPCRs can participate in various pathogenic process related to hearing loss in the cochlea including heredity, noise, ototoxic drugs, cochlear structure, and so on. In this review, we comprehensively summarize the functions of 53 GPCRs known in the cochlea and their relationships with hearing loss, and highlight the recent advances of new techniques used in cochlear study including cryo-EM, AI, GPCR drug screening, gene therapy vectors, and CRISPR editing technology, as well as discuss in depth the future direction of novel GPCR-based drug development and gene therapy for cochlear hearing loss. Collectively, this review is to facilitate basic and (pre-) clinical research in this area, and provide beneficial help for emerging GPCR-based cochlear therapies.