The role of inflammation and neurodegeneration in diabetic macular edema.

IF 2.3 Q2 OPHTHALMOLOGY Therapeutic Advances in Ophthalmology Pub Date : 2021-12-05 eCollection Date: 2021-01-01 DOI:10.1177/25158414211055963
Vincenzo Starace, Marco Battista, Maria Brambati, Michele Cavalleri, Federico Bertuzzi, Alessia Amato, Rosangela Lattanzio, Francesco Bandello, Maria Vittoria Cicinelli
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引用次数: 12

Abstract

The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.

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炎症和神经变性在糖尿病黄斑水肿中的作用。
糖尿病性黄斑水肿的发病机制是复杂的。持续高血糖激活多种细胞通路,诱发炎症、氧化应激和血管功能障碍。涉及视网膜神经节细胞、大胶质细胞和小胶质细胞、内皮细胞、周细胞和视网膜色素上皮细胞。以视网膜神经元功能障碍或凋亡丧失为特征的神经退行性变发生较早且独立于血管改变。尽管对二甲醚途径的了解越来越多,但只有有限的治疗策略可用。除了抗血管生成药物和玻璃体内皮质类固醇外,还考虑了治疗炎症、氧化应激和神经退行性变的替代治疗方案,但目前没有一种得到批准。
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来源期刊
CiteScore
4.50
自引率
0.00%
发文量
44
审稿时长
12 weeks
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