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瘦素作为青光眼的神经保护剂。

Leptin as a neuroprotective agent in glaucoma.

机构信息

Royal Derby Hospital, Uttoxeter Road, Derby, UK.

出版信息

Med Hypotheses. 2013 Nov;81(5):797-802. doi: 10.1016/j.mehy.2013.08.023. Epub 2013 Aug 29.

DOI:10.1016/j.mehy.2013.08.023
PMID:24035688
Abstract

Glaucoma is a disease characterized by progressive optic nerve degeneration and is the leading cause of irreversible blindness worldwide. More than 60 million people globally are affected by glaucoma, of which 8 million people suffer from bilateral blindness, making glaucoma the second leading cause of bilateral blindness worldwide. Current management of glaucoma is aimed at reducing intraocular pressure via a number of different strategies. Current treatments do not attempt to correct the underlying pathology of glaucoma, which is the cell degeneration and ultimate death of retinal ganglion cells, thereby limiting their clinical efficacy. A neuroprotective approach to glaucoma management would address the underlying pathology and would, in theory, be beneficial to all patients regardless of risk and causative factors. Here it is proposed that leptin could be used as a potential neuroprotective agent in the management of glaucoma. Leptin has shown neuroprotective promise in a number of neurodegenerative diseases, and there has been increasing evidence that glaucomatous neurodegeneration is analogous to other neurodegenerative diseases in the central nervous system. Leptin could target retinal ganglion cell death by a number of mechanisms, namely apoptosis, oxidative stress and excitotoxicity reduction. This article presents evidence linking current understanding about leptin's neuroprotective effect and the molecular mechanisms underlying glaucoma.

摘要

青光眼是一种以进行性视神经退行性病变为特征的疾病,是全球范围内导致不可逆性失明的主要原因。全球有超过 6000 万人受青光眼影响,其中 800 万人患有双眼盲,使青光眼成为全球第二大致盲原因。目前青光眼的治疗方法旨在通过多种不同策略降低眼内压。目前的治疗方法并没有试图纠正青光眼的潜在病理,即视网膜神经节细胞的变性和最终死亡,从而限制了其临床疗效。对青光眼进行神经保护治疗将针对潜在的病理,理论上对所有患者都有益,无论其风险和致病因素如何。本文提出瘦素可用作青光眼治疗中的一种潜在神经保护剂。瘦素在多种神经退行性疾病中显示出神经保护的潜力,并且越来越多的证据表明,青光眼性神经退行性变与中枢神经系统中的其他神经退行性疾病类似。瘦素可以通过多种机制靶向视网膜神经节细胞死亡,即细胞凋亡、氧化应激和兴奋毒性降低。本文介绍了将目前对瘦素神经保护作用的理解与青光眼的分子机制联系起来的证据。

相似文献

1
Leptin as a neuroprotective agent in glaucoma.瘦素作为青光眼的神经保护剂。
Med Hypotheses. 2013 Nov;81(5):797-802. doi: 10.1016/j.mehy.2013.08.023. Epub 2013 Aug 29.
2
Neuroprotection in glaucoma - Is there a future role?青光眼的神经保护治疗——是否有未来的作用?
Exp Eye Res. 2010 Nov;91(5):554-66. doi: 10.1016/j.exer.2010.08.009. Epub 2010 Aug 26.
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Neuroprotection in the treatment of glaucoma--A focus on connexin43 gap junction channel blockers.青光眼治疗中的神经保护——聚焦于连接蛋白43缝隙连接通道阻滞剂
Eur J Pharm Biopharm. 2015 Sep;95(Pt B):182-93. doi: 10.1016/j.ejpb.2015.01.031. Epub 2015 Feb 9.
4
Disease progression and the need for neuroprotection in glaucoma management.青光眼治疗中的疾病进展与神经保护需求。
Am J Manag Care. 2008 Feb;14(1 Suppl):S15-9.
5
Should we treat the brain in glaucoma?我们应该治疗青光眼患者的大脑吗?
Can J Ophthalmol. 2007 Jun;42(3):409-13.
6
Molecular and cell-based approaches for neuroprotection in glaucoma.青光眼神经保护的分子与细胞疗法
Optom Vis Sci. 2008 Jun;85(6):417-24. doi: 10.1097/OPX.0b013e31817841f7.
7
Neuroprotective therapies for glaucoma.青光眼的神经保护疗法。
Drug Des Devel Ther. 2015 Mar 11;9:1469-79. doi: 10.2147/DDDT.S80594. eCollection 2015.
8
Rational basis for the development of coenzyme Q10 as a neurotherapeutic agent for retinal protection.辅酶Q10作为视网膜保护神经治疗剂开发的合理依据。
Prog Brain Res. 2008;173:575-82. doi: 10.1016/S0079-6123(08)01139-4.
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[Retinal ganglion cells death in glaucoma--mechanism and potential treatment. Part I].[青光眼视网膜神经节细胞死亡——机制与潜在治疗方法。第一部分]
Klin Oczna. 2007;109(7-9):349-52.
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Neuroprotective Strategies in Glaucoma.青光眼的神经保护策略
Curr Pharm Des. 2016;22(14):2178-92. doi: 10.2174/1381612822666160128144747.

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