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近视是体内平衡的失败吗?

Is myopia a failure of homeostasis?

机构信息

Children's University Hospital, Department of Ophthalmology, Temple Street, Dublin 2, Ireland.

出版信息

Exp Eye Res. 2013 Sep;114:16-24. doi: 10.1016/j.exer.2013.02.008. Epub 2013 Feb 20.

Abstract

This review examines the hypothesis that human myopia is primarily a failure of homeostasis (i.e. regulated growth) and also considers the implications this has for research into refractive errors. There is ample evidence for homeostatic mechanisms in early life. During the first few years of life the eye grows toward emmetropia, a process called emmetropization. The key statistical features of this process are a shift of the mean population refraction toward emmetropia and a reduction in variability. Refractive errors result when either this process fails (primary homeostatic failure) or when an eye that becomes emmetropic fails to remain so during subsequent years (secondary homeostatic failure). A failure of homeostasis should increase variability as well as causing a possible shift in mean refraction. Increased variability is indeed seen in both animal models of myopia such as form deprivation and in human populations from the age of 5 or 6 onwards. Considering ametropia as a homeostatic failure also fits with the growing body of evidence that a wide range of factors and events can influence eye growth and refraction from gestation, through infancy, childhood and into adulthood. It is very important to recognize that the refraction of an eye is not a simple trait like eye colour but the consequence of the complex process of eye growth throughout life. To understand how an eye ends up with a specific refraction it is essential to understand all the factors that may promote the attainment and maintenance of emmetropia. Equally important are the factors that may either disrupt early emmetropization or lead to a loss of emmetropia during later development. Therefore, perhaps the most important single implication of a homeostatic view of myopia is that this condition is likely to have a very wide range of causes. This may allow us to identify subgroups of myopia for which specific environmental influences, genes or treatments can be found, effects that might be lost if all myopes are considered to be equivalent.

摘要

这篇综述探讨了一个假说,即人类近视主要是由于体内平衡(即调节性生长)的失败,同时也考虑了这一假说对屈光不正研究的影响。早期生活中有大量的体内平衡机制的证据。在生命的头几年,眼睛向正视方向生长,这个过程称为正视化。这个过程的关键统计特征是人群平均屈光度向正视方向的转移和变异性的降低。当这个过程失败(主要体内平衡失败)或已经正视的眼睛在随后的几年中无法保持正视时(次要体内平衡失败),就会出现屈光不正。体内平衡的失败不仅会导致平均屈光度可能发生变化,还会增加变异性。在近视的动物模型(如形觉剥夺)和 5 岁或 6 岁以上的人类群体中,确实都观察到了变异性的增加。将屈光不正视为体内平衡的失败也符合越来越多的证据,即从妊娠到婴儿期、儿童期和成年期,广泛的因素和事件都可以影响眼球生长和屈光度。非常重要的是要认识到,眼睛的屈光度不是像眼睛颜色那样简单的特征,而是眼睛在整个生命过程中生长的复杂过程的结果。要了解眼睛最终具有特定屈光度的原因,必须了解所有可能促进正视化的实现和维持的因素。同样重要的是,可能破坏早期正视化或导致后期发展中失去正视化的因素。因此,近视的体内平衡观点最重要的一个含义可能是,这种情况可能有非常广泛的原因。这可能使我们能够识别出特定的近视亚组,为这些亚组找到特定的环境影响、基因或治疗方法,如果将所有近视者视为等同,这些方法可能会丢失。

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