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Molecular pathology of inflammation in age‐related macular degeneration
Author(s) -
CHAN C
Publication year - 2012
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2012.3241.x
Subject(s) - inflammation , macular degeneration , immunology , chemokine , immune system , cx3cr1 , epigenetics , biology , genome wide association study , medicine , gene , genetics , chemokine receptor , single nucleotide polymorphism , genotype , ophthalmology
Purpose To review molecular pathology of inflammation in age‐related macular degeneration Methods Personal and collaborative research in addition to literature review Results Risk for AMD is multifactorial, relating to age, environmental and genetic factors. Genome‐wide and targeted genetic association studies have identified various polymorphisms important for AMD susceptibility. Many are within immune‐related genes, including complement factors, e.g. CFH, C2, C3, CFB, and CFI; Toll‐like receptors, e.g., TLR‐3 and TLR‐4; and chemokines and receptors, e.g., CX3CR1 and CCR3. In addition, copy number variation/polymorphism, miRNA and epigenetics related to immune relevant genes could also contribute to AMD pathogenesis and patient responses to specific therapies. Inflammatory cells (mainly macrophages and microglia) and inflammatory factors (complement factors, cytokines/chemokines, oxidative stress‐related inflammatory products) are demonstrated in AMD lesions at various stages. Conclusion The molecular characterization of AMD captures the localizations and interactions among the inflammatory elements, relevant molecules (e.g., oxidative stress products and lipoprotein), and retinal/choroidal cells, in particular, the photoreceptors and RPE.