ArticleThe American journal of pathology2011
Advanced glycation endproduct changes to Bruch's membrane promotes lipoprotein retention by lipoprotein lipase.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Age-related macular degeneration and cerebral amyloid angiopathy have similar pathologies from cholesterol-APOE-amyloid-β-complement mediated inflammation.Progress in retinal and eye research · 2026Review
- Age-Related Macular Degeneration: Cellular and Molecular Signaling Mechanisms.International journal of molecular sciences · 2025Review
- A histological study of atherosclerotic characteristics in age-related macular degeneration.Heliyon · 2022Article
- Age-related macular degeneration.Nature reviews. Disease primers · 2021Review
- Article
- Drusen and pachydrusen: the definition, pathogenesis, and clinical significance.Eye (London, England) · 2021Review
- Bruch's Membrane and the Choroid in Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2021Article
- A systems biology approach towards understanding and treating non-neovascular age-related macular degeneration.Nature communications · 2019Review
- The impact of lipids, lipid oxidation, and inflammation on AMD, and the potential role of miRNAs on lipid metabolism in the RPE.Experimental eye research · 2019Review
- The Association Between Variants of Receptor for Advanced Glycation End Products (RAGE) Gene Polymorphisms and Age-Related Macular Degeneration.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Mast Cell-Derived Tryptase in Geographic Atrophy.Investigative ophthalmology & visual science · 2017Article
- The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD.Progress in retinal and eye research · 2017Review
- Correlations between Photodegradation of Bisretinoid Constituents of Retina and Dicarbonyl Adduct Deposition.The Journal of biological chemistry · 2015Article
- Article
- Mice that produce ApoB100 lipoproteins in the RPE do not develop drusen yet are still a valuable experimental system.Investigative ophthalmology & visual science · 2014Article
- Fundus Autofluorescence and RPE Lipofuscin in Age-Related Macular Degeneration.Journal of clinical medicine · 2014Article
- Understanding RPE lipofuscin.Investigative ophthalmology & visual science · 2013Article
- Complement dysregulation in AMD: RPE-Bruch's membrane-choroid.Molecular aspects of medicine · 2012Review
- How does the macula protect itself from oxidative stress?Molecular aspects of medicine · 2012Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Lipoprotein particles accumulate in Bruch's membrane before the development of basal deposits and drusen, two histopathologic lesions that define age-related macular degeneration (AMD). We therefore, sought to determine which molecules could participate in lipoprotein retention. Wild-type or lipoprotein lipase-deficient mice were injected with low-dose D-galactose or PBS subcutaneously for 8 weeks to induce advanced glycation endproduct (AGE) formation. Some mice were also injected with the AGE breaker phenacylphiazolium bromide and D-galactose. Rhodamine-labeled low-density lipoproteins were injected into mice, and the fluorescence was measured up to 72 hours later. AGEs, proteoglycans, and other lipid-retaining molecules were evaluated by IHC. Lipoprotein lipase distribution was assessed in AMD samples by IHC. D-galactose-treated mice retained lipoproteins in the retinal pigment epithelial and Bruch's membrane to a greater extent than either PBS- or phenacylphiazolium bromide/D-galactose-treated mice at 24 and 72 hours after injection (P ≤ 0.04). Immunolabeling for carboxymethyllysine, biglycan, and lipoprotein lipase was found in D-galactose-treated mice only. Mice deficient for lipoprotein lipase treated with D-galactose did not retain lipoproteins to any measureable extent. Human AMD samples had lipoprotein lipase labeling within drusen, basal deposits, and the choroid. Mice treated with D-galactose to induce AGE formation in Bruch's membrane retain intravenously injected lipoproteins. Our results suggest that lipoprotein retention in Bruch's membrane is mediated by lipoprotein lipase.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.