ArticleMolecular & cellular proteomics : MCP2010
Quantitative proteomics: comparison of the macular Bruch membrane/choroid complex from age-related macular degeneration and normal eyes.
Article in Molecular & cellular proteomics : MCP, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.
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Who cites it
102 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.
- Recent Advances in Proteomics-Based Approaches to Studying Age-Related Macular Degeneration: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Systemic complement activation levels in Stargardt disease.PloS one · 2021Trial
- Retinal proteomics in neurodegeneration: Insights into ocular and brain disorders.Neural regeneration research · 2026Article
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- Characterization of the Effects of a Humanin Fragment Peptide (HNFJournal of clinical medicine · 2026Article
- Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Article
- Role of Endogenous Galectin-3 on Cell Biology of Immortalized Retinal Pigment Epithelial Cells In Vitro.International journal of molecular sciences · 2025Article
- Decreased complement 4 and interleukin-10 as biomarkers in aqueous humour for non-exudative age-related macular degeneration: a case control study.Journal of translational medicine · 2025Article
- Sigma-2 receptor modulator CT1812 alters key pathways and rescues retinal pigment epithelium (RPE) functional deficits associated with dry age-related macular degeneration (AMD).Scientific reports · 2025Article
- Article
- Ocular Localization of Complement Factor H and Its Association with Diseases in the Eye.Advances in experimental medicine and biology · 2025Review
- Loss of Pigment Epithelium Derived Factor Sensitizes C57BL/6J Mice to Light-Induced Retinal Damage.bioRxiv : the preprint server for biology · 2024Article
- Involvement ofBiomedicines · 2024Article
- Ghost vessels in the eye: Cell free choriocapillaris domains in atrophic age-related macular degeneration.Experimental eye research · 2024Article
- Quantitative proteomic profiling reveals sexual dimorphism in the retina and RPE of C57BL6 mice.Biology of sex differences · 2024Article
- CD6 triggers actomyosin cytoskeleton remodeling after binding to its receptor complex.Journal of leukocyte biology · 2024Article
- The Role of Galectin-3 in Retinal Degeneration and Other Ocular Diseases: A Potential Novel Biomarker and Therapeutic Target.International journal of molecular sciences · 2023Review
- The Role of Inflammation in Age-Related Macular Degeneration-Therapeutic Landscapes in Geographic Atrophy.Cells · 2023Review
- Oxidative stress induces lysosomal membrane permeabilization and ceramide accumulation in retinal pigment epithelial cells.Disease models & mechanisms · 2023Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
A quantitative proteomics analysis of the macular Bruch membrane/choroid complex was pursued for insights into the molecular mechanisms of age-related macular degeneration (AMD). Protein in trephine samples from the macular region of 10 early/mid-stage dry AMD, six advanced dry AMD, eight wet AMD, and 25 normal control post-mortem eyes was analyzed by LC MS/MS iTRAQ (isobaric tags for relative and absolute quantitation) technology. A total of 901 proteins was quantified, including 556 proteins from > or =3 AMD samples. Most proteins differed little in amount between AMD and control samples and therefore reflect the proteome of normal macular tissues of average age 81. A total of 56 proteins were found to be elevated and 43 were found to be reduced in AMD tissues relative to controls. Analysis by category of disease progression revealed up to 16 proteins elevated or decreased in each category. About 60% of the elevated proteins are involved in immune response and host defense, including many complement proteins and damage-associated molecular pattern proteins such as alpha-defensins 1-3, protein S100s, crystallins, histones, and galectin-3. Four retinoid processing proteins were elevated only in early/mid-stage AMD, supporting a role for retinoids in AMD initiation. Proteins uniquely decreased in early/mid-stage AMD implicate hematologic malfunctions and weakened extracellular matrix integrity and cellular interactions. Galectin-3, a receptor for advanced glycation end products, was the most significantly elevated protein in advanced dry AMD, supporting a role for advanced glycation end products in dry AMD progression. The results endorse inflammatory processes in both early and advanced AMD pathology, implicate different pathways of progression to advanced dry and wet AMD, and provide a new database for hypothesis-driven and discovery-based studies of AMD.
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