Introduction
Sensorineural hearing loss (SNHL) afflicts over 1.5 billion people worldwide and represents a leading cause of disability. Its multifactorial etiology encompasses genetic mutations, environmental insults such as noise exposure, ototoxic drugs, aging, and viral infections. Increasing evidence implicates the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome as a pivotal driver of inflammation-induced cochlear damage underlying many SNHL forms. The dysregulated activation of this innate immune complex triggers a cascade of proinflammatory cytokine release and pyroptotic cell death, contributing to progressive and often irreversible auditory dysfunction. This article critically reviews the mechanistic roles of the NLRP3 inflammasome in diverse hearing loss etiologies and highlights emerging therapeutic candidates targeting this pathway with translational potential.
