The ocular surface structure and extraocular accessory organs constitute the ocular surface system, which includes the cornea, conjunctiva, eyelids, lacrimal organs, and lacrimal passages. This system is composed of, and stabilized by, the corneal epithelium, conjunctival cells, conjunctival goblet cells, lacrimal acinar cells and Tenon’s fibroblasts, all of which maintain the healthy eyeball surface system. Ocular surface diseases are commonly referred to corneal and conjunctival disease and external ocular disease, resulting from damage to the ocular surface structure. A growing body of evidence has indicated that abnormal activation of the KCa3.1 channel and Ca2+/ calmodulin-dependent kinase initiates ocular injury. Signaling pathways downstream of the irregular Ca2+ influx induce cell progression and migration, and impair tight junctions, epithelial transport and secretory function. In this overview, we summarize the current knowledge regarding ocular surface disease in terms of physical and pathological alteration of the ocular system. We dissect in-depth, the mechanisms underlying disease progression, and we describe the current calcium transport therapeutics and the obstacles that remain to be solved. Finally, we summarize how to integrate the research results into clinical practice in the future.

眼表结构和眼外附属器官构成眼表系统，其中包括角膜，结膜，眼睑，泪腺器官和泪道。该系统由角膜上皮，结膜细胞，结膜杯状细胞，泪腺腺泡细胞和Tenon成纤维细胞组成并由其稳定，所有这些都维持着健康的眼球表面系统。眼表疾病通常是指由于对眼表结构的损害而导致的角膜和结膜疾病和外眼疾病。越来越多的证据表明，KCa3.1通道和Ca2 + /钙调蛋白依赖性激酶的异常激活会引发眼损伤。不规则Ca2 +流入下游的信号通路会诱导细胞进程和迁移，并削弱紧密连接，上皮运输和分泌功能。在本概述中，我们根据眼系统的物理和病理变化总结了有关眼表疾病的当前知识。我们深入剖析了疾病进展的潜在机制，并描述了当前的钙转运疗法和仍有待解决的障碍。最后，我们总结了将来如何将研究结果整合到临床实践中。