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Hypothesis Of K+-Recycling Defect Is Not A Primary Deafness Mechanism For Cx26 (Gjb2) Deficiency, Hong-Bo Zhao
Hypothesis Of K+-Recycling Defect Is Not A Primary Deafness Mechanism For Cx26 (Gjb2) Deficiency, Hong-Bo Zhao
Otolaryngology--Head & Neck Surgery Faculty Publications
K+-recycling defect is a long-standing hypothesis for deafness mechanism of Connexin26 (Cx26, GJB2) mutations, which cause the most common hereditary deafness and are responsible for >50% of nonsyndromic hearing loss. The hypothesis states that Cx26 deficiency may disrupt inner ear gap junctions and compromise sinking and recycling of expelled K+ ions after hair cell excitation, causing accumulation of K+-ions in the extracellular space around hair cells producing K+-toxicity, which eventually induces hair cell degeneration and hearing loss. However, this hypothesis has never been directly evidenced, even though it has been widely referred …