59TH INNER EAR BIOLOGY WORKSHOP, 15–17 SEPTEMBER 2024, WARSAW, POLAND
Cellular senescence, a state of permanent cell cycle arrest, is vital in embryonic development, including inner ear formation.During this process, senescent cells aid morphogenesis by regulating tissue remodeling and ensuring proper cell differentiation.Senescent cells are characterized by distinctive morphological and physiological changes, including enlarged cell size, increased -galactosidase activity, altered gene expression, and the secretion of various inflammatory cytokines, chemokines, and proteases, collectively known as the senescence-associated secretory phenotype (SASP).Senescence cells secrete factors that shape the development of auditory structures like the cochlea and vestibular apparatus.Deficits in embryonic senescence can lead to malformations and functional impairments in the inner ear.This highlights the importance of regulated senescence for proper inner ear development.Vestibular schwannomas, age-associated benign tumors from Schwann cells of the vestibular nerve, further illustrate senescence's role in ear health.These tumors can cause hearing loss, tinnitus, and balance issues.In tumors, senescence can both suppress and promote growth.While senescence halts uncontrolled cell proliferation, the senescence-associated secretory phenotype (SASP) can create a pro-tumorigenic environment, enhancing tumor survival and progression.Understanding senescence's dual roles in embryonic development and tumorigenesis is crucial for targeted therapies.In embryonic contexts, promoting proper senescence could prevent anomalies.In vestibular schwannomas, modulating senescence and SASP factors may improve outcomes, indicating the potential for senescencetargeted interventions in developmental and neoplastic inner ear conditions.
Publication Details
- Journal
- Journal of Hearing Science
- Published
- 2024-09-05
- DOI
- https://doi.org/10.17430/jhs/192760
- Primary Topic
- Hearing, Cochlea, Tinnitus, Genetics
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Deutsche Forschungsgemeinschaft
- Bundesministerium für Bildung und Forschung
- Fonds Wetenschappelijk Onderzoek