[关键词]
[摘要]
全球近视发病率持续攀升,世界卫生组织预测本世纪中叶将有一半人口受近视影响,缓解全球近视“流行”问题迫在眉睫。近视不仅导致视力下降,更与青光眼、视网膜病变等不可逆性致盲疾病密切相关,其病理机制与眼压(IOP)对巩膜结构的生物力学作用存在重要关联。近视发展过程中,巩膜组织呈现显著的结构重塑,使其对眼压的机械应力更为敏感。关键机制包括基质金属蛋白酶-2(MMP-2)活性增强加速胶原降解,其特异性抑制剂(TIMPs)的调控失衡导致细胞外基质动态稳定性破坏; 缺氧诱导因子-1α(HIF-1α)通路激活引发的脉络膜血供异常,以及PI3K/AKT信号通路在巩膜重塑中的级联调控作用。文章系统梳理眼压变化与近视进展的关系及其分子机制,为进一步探究近视防控的方式方法提供了重要的科学基础和新思路。
[Key word]
[Abstract]
Myopia prevalence is still rising worldwide, addressing the worldwide myopia “epidemic” is of utmost importance, since the World Health Organization estimates that half of the world's population will suffer from myopia by the middle of the century. In addition to causing vision loss, myopia is closely associated with irreversible blinding disorders such as glaucoma and retinopathy. The pathophysiology of myopia is strongly linked to the biomechanical effects of intraocular pressure(IOP)on the scleral structure. Scleral tissue undergoes considerable structural remodelling during myopia development, increasing its sensitivity to the mechanical stresses of IOP. Important mechanisms include increased collagen degradation brought on by matrix metalloproteinase(MMP-2)activity, extracellular matrix dynamics destabilization from an imbalance in the regulation of tissue inhibitor of metalloproteinase(TIMPs), aberrant choroidal blood supply brought on by activation of the hypoxia-inducible factor-1α(HIF-1α)pathway, and cascading regulation of the PI3K/AKT signaling pathway in scleral remodeling. This study provides a significant scientific foundation and fresh concepts for the future research into myopia prevention and control strategies by methodically examining the connection between changes in IOP and the development of myopia as well as its molecular underpinnings.
[中图分类号]
[基金项目]
山东省医药卫生科技发展计划项目(No.202207020770); 山东中医药科技项目(No.M-2022165); 山东省医药卫生科技项目(No.202307021577)