Shindler Kenneth S
Department of Ophthalmology, University of Pennsylvania, Scheie Eye Institute, Philadelphia, PA, USA. Email:
Ophthalmol Eye Dis. 2009 Nov 17;1:41-3. doi: 10.4137/oed.s3417. Print 2009.
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.
一些研究表明，基于观察到的高半胱氨酸水平升高与视网膜病变的存在之间的相关性，高半胱氨酸可能是糖尿病患者视网膜病变发展的一个促成因素。这种相关性的意义仍有待确定，高半胱氨酸可能诱发视网膜病变的潜在机制尚未得到充分描述。加纳帕蒂及其同事利用由于胱硫醚-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，来研究糖尿病诱导后视网膜病理学的变化。他们发现高半胱氨酸水平升高会加速视网膜神经节细胞层细胞的丢失，这表明对神经节细胞的毒性作为高半胱氨酸增强糖尿病视网膜病变易感性的潜在机制，可能值得进一步研究。
