| Literature DB >> 26427398 |
Luciana M Pujol-Lereis1, Nicole Schäfer2, Laura B Kuhn3, Bärbel Rohrer4, Diana Pauly5.
Abstract
Millions of individuals older than 50-years suffer from age-related macular degeneration (AMD). Associated with this multifactorial disease are polymorphisms of complement factor genes and a main environmental risk factor-oxidative stress. Until now the linkage between these risk factors for AMD has not been fully understood. Recent studies, integrating results on oxidative stress, complement activation, epidemiology and ocular pathology suggested the following sequence in AMD-etiology: initially, chronic oxidative stress results in modification of proteins and lipids in the posterior of the eye; these tissue alterations trigger chronic inflammation, involving the complement system; and finally, invasive immune cells facilitate pathology in the retina. Here, we summarize the results for animal studies which aim to elucidate this molecular interplay of oxidative events and tissue-specific complement activation in the eye.Entities:
Keywords: Age-related macular degeneration; Alternative pathway; CEP-immunization model; Cigarette smoke model; Complement system; Knock-out mice models; Light-damage model; Oxidation-specific epitopes; Oxidative stress; Sodium iodate-treatment model
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Year: 2016 PMID: 26427398 DOI: 10.1007/978-3-319-17121-0_13
Source DB: PubMed Journal: Adv Exp Med Biol ISSN: 0065-2598 Impact factor: 2.622