Department of Otolaryngology-Head and Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Physiol Res. 2020 Nov 16;69(5):775-785. doi: 10.33549/physiolres.934447. Epub 2020 Sep 9.
Sensorineural hearing loss and vertigo, resulting from lesions in the sensory epithelium of the inner ear, have a high incidence worldwide. The sensory epithelium of the inner ear may exhibit extreme degeneration and is transformed to flat epithelium (FE) in humans and mice with profound sensorineural hearing loss and/or vertigo. Various factors, including ototoxic drugs, noise exposure, aging, and genetic defects, can induce FE. Both hair cells and supporting cells are severely damaged in FE, and the normal cytoarchitecture of the sensory epithelium is replaced by a monolayer of very thin, flat cells of irregular contour. The pathophysiologic mechanism of FE is unclear but involves robust cell division. The cellular origin of flat cells in FE is heterogeneous; they may be transformed from supporting cells that have lost some features of supporting cells (dedifferentiation) or may have migrated from the flanking region. The epithelial-mesenchymal transition may play an important role in this process. The treatment of FE is challenging given the severe degeneration and loss of both hair cells and supporting cells. Cochlear implant or vestibular prosthesis implantation, gene therapy, and stem cell therapy show promise for the treatment of FE, although many challenges remain to be overcome.
感音神经性听力损失和眩晕是由于内耳感觉上皮的病变引起的，在全球范围内发病率很高。内耳感觉上皮可能会出现极度退化，并在严重感音神经性听力损失和/或眩晕的人类和小鼠中转化为扁平上皮（FE）。各种因素，包括耳毒性药物、噪声暴露、衰老和遗传缺陷，都可以诱导 FE 的发生。FE 中毛细胞和支持细胞都受到严重损伤，感觉上皮的正常细胞结构被单层非常薄、形态不规则的扁平细胞所取代。FE 的病理生理机制尚不清楚，但涉及到强烈的细胞分裂。FE 中扁平细胞的细胞来源是异质的；它们可能是由失去某些支持细胞特征的支持细胞（去分化）转化而来，也可能是从毗邻区域迁移而来。上皮-间充质转化可能在此过程中起重要作用。由于毛细胞和支持细胞都严重退化和丧失，FE 的治疗具有挑战性。尽管还有许多挑战需要克服，但耳蜗植入或前庭假体植入、基因治疗和干细胞治疗在治疗 FE 方面显示出了希望。
