Cochlear Inflammatory Microenvironment in Age-Related Hearing Loss: Mechanisms and Recent Advances

Age-related hearing loss (ARHL) is a common sensory disorder in older adults and a major public health concern that reduces quality of life and social functioning. Traditionally, ARHL has been associated with hair cell apoptosis, strial degeneration, spiral ganglion neuron loss, oxidative stress, and mitochondrial dysfunction. Recent studies suggest that dysregulation of the cochlear inflammatory microenvironment also contributes to its onset and progression. During aging, impaired immune regulation, weakened antioxidant defenses, blood-labyrinth barrier dysfunction, and persistent pro-inflammatory signaling disturb cochlear homeostasis and promote pathological remodeling, leading to injury of hair cells, synapses, and auditory neurons. In addition, systemic chronic low-grade inflammation, metabolic disturbances, and vascular dysfunction may further worsen cochlear inflammation. This review summarizes the structural basis, maladaptive remodeling, functional consequences, and potential therapeutic strategies of the cochlear inflammatory microenvironment in ARHL.