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[年龄相关性黄斑变性作为一种血管疾病/系统性血管病变的一部分:对其发病机制的贡献]

[The age-related macular degeneration as a vascular disease/part of systemic vasculopathy: contributions to its pathogenesis].

作者信息

Fischer Tamás

机构信息

Budapest Körvasút sor 75/B 1158.

出版信息

Orv Hetil. 2015 Mar 1;156(9):358-65. doi: 10.1556/OH.2015.30017.

DOI:10.1556/OH.2015.30017
PMID:25702256
Abstract

The wall of blood vessels including those in choroids may be harmed by several repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic, and genetic impacts (risk factors), which may trigger a protracted response, the so-called host defense response. As a consequence, pathological changes resulting in vascular injury (e. g. atherosclerosis, age-related macular degeneration) may be evolved. Risk factors can also act directly on the endothelium through an increased production of reactive oxygen species promoting an endothelial activation, which leads to endothelial dysfunction, the onset of vascular disease. Thus, endothelial dysfunction is a link between the harmful stimulus and vascular injury; any kind of harmful stimuli may trigger the defensive chain that results in inflammation that may lead to vascular injury. It has been shown that even early age-related macular degeneration is associated with the presence of diffuse arterial disease and patients with early age-related macular degeneration demonstrate signs of systemic and retinal vascular alterations. Chronic inflammation, a feature of AMD, is tightly linked to diseases associated with ED: AMD is accompanied by a general inflammatory response, in the form of complement system activation, similar to that observed in degenerative vascular diseases such as atherosclerosis. All these facts indicate that age-related macular degeneration may be a vascular disease (or part of a systemic vasculopathy). This recognition could have therapeutic implications because restoration of endothelial dysfunction may prevent the development or improve vascular disease resulting in prevention or improvement of age-related macular degeneration as well.

摘要

血管壁,包括脉络膜中的血管壁,可能会受到几种反复和/或长期的机械、物理、化学、微生物、免疫和遗传影响(风险因素)的损害,这些影响可能引发一种持久的反应,即所谓的宿主防御反应。结果,可能会出现导致血管损伤的病理变化(例如动脉粥样硬化、年龄相关性黄斑变性)。风险因素还可通过增加活性氧的产生直接作用于内皮细胞,促进内皮细胞活化,从而导致内皮功能障碍和血管疾病的发生。因此,内皮功能障碍是有害刺激与血管损伤之间的联系;任何一种有害刺激都可能触发导致炎症的防御链,进而可能导致血管损伤。研究表明,即使是早期年龄相关性黄斑变性也与弥漫性动脉疾病的存在有关,并且早期年龄相关性黄斑变性患者表现出全身和视网膜血管改变的迹象。慢性炎症是年龄相关性黄斑变性的一个特征,与内皮功能障碍相关的疾病密切相关:年龄相关性黄斑变性伴随着以补体系统激活形式出现的全身性炎症反应,类似于在动脉粥样硬化等退行性血管疾病中观察到的炎症反应。所有这些事实表明,年龄相关性黄斑变性可能是一种血管疾病(或全身性血管病变的一部分)。这种认识可能具有治疗意义,因为恢复内皮功能障碍可能预防血管疾病的发展或改善血管疾病,从而也预防或改善年龄相关性黄斑变性。

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