糖尿病视网膜神经节细胞损失与高半胱氨酸升高有关。

Ophthalmology and eye diseases Pub Date : 2009-11-17 Print Date: 2009-01-01 DOI:10.4137/oed.s3417
Kenneth S Shindler
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引用次数: 1

摘要

许多研究表明,根据观察到的高同型半胱氨酸水平与视网膜病变存在的相关性,同型半胱氨酸可能是糖尿病患者视网膜病变发展的一个促进因素。这种相关性的重要性仍有待确定,同型半胱氨酸可能诱发视网膜病变的潜在机制尚未得到很好的表征。Ganapathy和他的同事们1使用由于胱氨酸-β合酶基因杂合缺失而内源性高半胱氨酸水平升高的突变小鼠来检测糖尿病诱导后视网膜病理的变化。他们发现,高同型半胱氨酸水平加速视网膜神经节细胞层细胞的损失,这表明对神经节细胞的毒性可能值得进一步研究,作为同型半胱氨酸增加糖尿病视网膜病变易感性的潜在机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Retinal ganglion cell loss in diabetes associated with elevated homocysteine.

A number of studies have suggested that homocysteine may be a contributing factor to development of retinopathy in diabetic patients based on observed correlations between elevated homocysteine levels and the presence of retinopathy. The significance of such a correlation remains to be determined, and potential mechanisms by which homocysteine might induce retinopathy have not been well characterized. Ganapathy and colleagues1 used mutant mice that have endogenously elevated homocysteine levels due to heterozygous deletion of the cystathionine-β-synthase gene to examine changes in retinal pathology following induction of diabetes. Their finding that elevated homocysteine levels hastens loss of cells in the retinal ganglion cell layer suggests that toxicity to ganglion cells may warrant further investigation as a potential mechanism of homocysteine enhanced susceptibility to diabetic retinopathy.

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