Age-related hearing loss (ARHL) is the most prevalent sensory deficit in the elderly and constitutes the third highest risk factor for dementia. Lifetime noise exposure, genetic predispositions for degeneration, and metabolic stress are assumed to be the major causes of ARHL. Both noise-induced and hereditary progressive hearing have been linked to decreased cell surface expression and impaired conductance of the potassium ion channel K_V7.4 (KCNQ4) in outer hair cells, inspiring future therapies to maintain or prevent the decline of potassium ion channel surface expression to reduce ARHL. In concert with K_V7.4 in outer hair cells, K_V7.1 (KCNQ1) in the stria vascularis, calcium-activated potassium channels BK (KCNMA1) and SK2 (KCNN2) in hair cells and efferent fiber synapses, and K_V3.1 (KCNC1) in the spiral ganglia and ascending auditory circuits share an upregulated expression or subcellular targeting during final differentiation at hearing onset. They also share a distinctive fragility for noise exposure and age-dependent shortfalls in energy supply required for sustained surface expression. Here, we review and discuss the possible contribution of select potassium ion channels in the cochlea and auditory pathway to ARHL. We postulate genes, proteins, or modulators that contribute to sustained ion currents or proper surface expressions of potassium channels under challenging conditions as key for future therapies of ARHL.

年龄相关性听力损失 (ARHL) 是老年人最普遍的感觉障碍，是痴呆症的第三高风险因素。终生暴露于噪音、遗传易感性退化和代谢压力被认为是 ARHL 的主要原因。噪声诱导和遗传性进行性听力都与外毛细胞中的细胞表面表达降低和钾离子通道 K _V 7.4 (KCNQ4) 的电导受损有关，从而激发未来的治疗方法以维持或防止钾离子通道表面表达的下降以减少 ARHL。与外毛细胞中的K _V 7.4 一致，K _V血管纹中的 7.1 (KCNQ1)、毛细胞和传出纤维突触中的钙激活钾通道 BK (KCNMA1) 和 SK2 (KCNN2) 以及螺旋神经节和上行听觉回路中的K _V 3.1 (KCNC1) 共享一个上调的表达或在听力开始时的最终分化过程中进行亚细胞靶向。它们在暴露于噪音和与年龄相关的持续表面表达所需的能量供应方面也具有独特的脆弱性。在这里，我们回顾并讨论了耳蜗和听觉通路中选择的钾离子通道对 ARHL 的可能贡献。我们假设在具有挑战性的条件下有助于持续离子流或钾通道适当表面表达的基因、蛋白质或调节剂是 ARHL 未来治疗的关键。