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[视网膜缺血的分子机制]

[Molecular mechanisms of retinal ischemia].

作者信息

Neroev V V, Zueva M V, Kalamkarov G R

出版信息

Vestn Oftalmol. 2010 May-Jun;126(3):59-64.

Abstract

The review discusses the molecular mechanisms of retinal damage, which are associated with retinal ischemia. Ischemia is one of the key factors determining the pathophysiology of many retinal diseases, such as diabetic retinopathy, glaucoma, anterior ischemic optic neuropathy, age-related macular degeneration, retinopathy of prematurity. Hypoxia and ischemia impair retinal neuronal energy metabolism, by launching a cascade of trigger reactions resulting in cell death. Oxidative stress, excitotoxicity, cell acidosis, inflammation, and others mechanisms acting in tandem are of considerable importance in ischemia. Neuronal apoptosis and neovascularization are the most important sequels of ischemia. Among all retinal neurons, ganglion cells are most susceptible to ischemia, which determines their early structural and functional changes in many ischemia-associated retinal diseases. The molecular mechanisms underlying the pathophysiology of ischemia-associated retinal diseases should be understood to substantiate and develop new therapy modalities.

摘要

该综述讨论了与视网膜缺血相关的视网膜损伤的分子机制。缺血是决定许多视网膜疾病病理生理学的关键因素之一,如糖尿病性视网膜病变、青光眼、前部缺血性视神经病变、年龄相关性黄斑变性、早产儿视网膜病变。缺氧和缺血通过引发一系列触发反应导致细胞死亡,从而损害视网膜神经元的能量代谢。氧化应激、兴奋性毒性、细胞酸中毒、炎症以及其他协同作用的机制在缺血中具有相当重要的意义。神经元凋亡和新生血管形成是缺血最重要的后果。在所有视网膜神经元中,神经节细胞对缺血最为敏感,这决定了它们在许多与缺血相关的视网膜疾病中的早期结构和功能变化。为了证实和开发新的治疗方法,应该了解缺血相关视网膜疾病病理生理学的分子机制。

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