Lipids, oxidized lipids, oxidation-specific epitopes, and Age-related Macular Degeneration

被引:84
作者
Handa, James T. [1 ]
Cano, Marisol [1 ]
Wang, Lei [1 ]
Datta, Sayantan [1 ]
Liu, Tongyun [1 ]
机构
[1] Johns Hopkins Sch Med, Wilmer Eye Inst, Baltimore, MD 21287 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS | 2017年 / 1862卷 / 04期
关键词
Age-related Macular Degeneration; Bruch's membrane; Basal deposits; Drusen; Very low-density lipoprotein (LDL); Oxidation-specific epitopes; Retinal pigmented epithelium (RPE); RETINAL-PIGMENT EPITHELIUM; COMPLEMENT FACTOR-H; SUBRETINAL DRUSENOID DEPOSITS; GENOME-WIDE ASSOCIATION; LOW-DENSITY-LIPOPROTEIN; LONG-TERM INCIDENCE; NF-KAPPA-B; RETICULAR PSEUDODRUSEN; 5-YEAR INCIDENCE; RISK-FACTORS;
D O I
10.1016/j.bbalip.2016.07.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Age-related Macular Degeneration (AMD) is the leading cause of blindness among the elderly in western societies. While antioxidant micronutrient treatment is available for intermediate non-neovascular disease, and effective anti-vascular endothelial growth factor treatment is available for neovascular disease, treatment for early AMD is lacking due to an incomplete understanding of the early molecular events. The role of lipids, which accumulate in the macula, and their oxidation, has emerged as an important factor in disease development. These oxidized lipids can either directly contribute to tissue injury or react with amine on proteins to form oxidation-specific epitopes, which can induce an innate immune response. If inadequately neutralized, the inflammatory response from these epitopes can incite tissue injury during disease development. This review explores how the accumulation of lipids, their oxidation, and the ensuing inflammatory response might contribute to the pathogenesis of AMD. This article is part of a Special Issue entitled: Lipid modification and lipid peroxidation products in innate immunity and inflammation edited by Christoph J. Binder. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:430 / 440
页数:11
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