Universitätsaugenklinik / IZKF Aachen, RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany.
Curr Genomics. 2012 Aug;13(5):350-62. doi: 10.2174/138920212801619214.
Retinal degenerations encompass a large number of diseases in which the retina and associated retinal pigment epithelial (RPE) cells progressively degenerate leading to severe visual disorders or blindness. Retinal degenerations can be divided into two groups, a group in which the defect has been linked to a specific gene and a second group that has a complex etiology that includes environmental and genetic influences. The first group encompasses a number of relatively rare diseases with the most prevalent being Retinitis pigmentosa that affects approximately 1 million individuals worldwide. Attempts have been made to correct the defective gene by transfecting the appropriate cells with the wild-type gene and while these attempts have been successful in animal models, human gene therapy for these inherited retinal degenerations has only begun recently and the results are promising. To the second group belong glaucoma, age-related macular degeneration (AMD) and diabetic retinopathy (DR). These retinal degenerations have a genetic component since they occur more often in families with affected probands but they are also linked to environmental factors, specifically elevated intraocular pressure, age and high blood sugar levels respectively. The economic and medical impact of these three diseases can be assessed by the number of individuals affected; AMD affects over 30 million, DR over 40 million and glaucoma over 65 million individuals worldwide. The basic defect in these diseases appears to be the relative lack of a neurogenic environment; the neovascularization that often accompanies these diseases has suggested that a decrease in pigment epithelium-derived factor (PEDF), at least in part, may be responsible for the neurodegeneration since PEDF is not only an effective neurogenic and neuroprotective agent but also a potent inhibitor of neovascularization. In the last few years inhibitors of vascularization, especially antibodies against vascular endothelial cell growth factors (VEGF), have been used to prevent the neovascularization that accompanies AMD and DR resulting in the amelioration of vision in a significant number of patients. In animal models it has been shown that transfection of RPE cells with the gene for PEDF and other growth factors can prevent or slow degeneration. A limited number of studies in humans have also shown that transfection of RPE cells in vivo with the gene for PEDF is effective in preventing degeneration and restore vision. Most of these studies have used virally mediated gene delivery with all its accompanying side effects and have not been widely used. New techniques using non-viral protocols that allow efficient delivery and permanent integration of the transgene into the host cell genome offer novel opportunities for effective treatment of retinal degenerations.
视网膜变性包括一大类疾病,这些疾病导致视网膜和相关的视网膜色素上皮(RPE)细胞进行性退化,从而导致严重的视力障碍或失明。视网膜变性可以分为两组,一组是缺陷与特定基因相关,另一组是具有复杂病因的疾病,包括环境和遗传因素。第一组包括许多相对罕见的疾病,其中最常见的是色素性视网膜炎,影响全球约 100 万人。人们试图通过用野生型基因转染适当的细胞来纠正有缺陷的基因,虽然这些尝试在动物模型中取得了成功,但针对这些遗传性视网膜变性的人体基因治疗最近才刚刚开始,并且结果很有前景。第二类疾病包括青光眼、年龄相关性黄斑变性(AMD)和糖尿病性视网膜病变(DR)。这些视网膜变性具有遗传成分,因为它们在有受影响先证者的家族中更常见,但它们也与环境因素有关,具体而言,分别与眼内压升高、年龄和高血糖水平有关。可以通过受影响的个体数量来评估这三种疾病的经济和医疗影响;AMD 影响超过 3000 万人,DR 影响超过 4000 万人,青光眼影响超过全球 6500 万人。这些疾病的基本缺陷似乎是相对缺乏神经营养环境;这些疾病常伴有新生血管化,这表明至少部分原因是色素上皮衍生因子(PEDF)的减少,因为 PEDF 不仅是一种有效的神经营养和神经保护剂,也是新生血管化的有效抑制剂。在过去几年中,血管生成抑制剂,特别是针对血管内皮细胞生长因子(VEGF)的抗体,已被用于预防 AMD 和 DR 伴随的新生血管化,从而改善了大量患者的视力。在动物模型中,已经表明用 PEDF 和其他生长因子的基因转染 RPE 细胞可以预防或减缓变性。在人体中进行的少数研究也表明,用 PEDF 的基因转染 RPE 细胞在体内是有效的,可预防变性并恢复视力。这些研究大多使用病毒介导的基因传递,伴随所有伴随的副作用,并未广泛使用。使用允许有效递送电基因并将转基因永久整合到宿主细胞基因组中的新非病毒方案为有效治疗视网膜变性提供了新的机会。