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The cellular and molecular pathogenesis of initiation and development of AMD remain poorly delineated. The limited resources of the human AMD RPE\/choroid tissues impeded the extensive study of the disease. To better understand the molecular and pathway changes in human AMD RPE\/choroid tissues, we searched the literature and found three independent studies using high-throughput technology to analyze gene expression in 54 human AMD RPE\/choroid tissues and 46 age-matched healthy controls. We downloaded these data, pooled them together, and reanalyzed the difference between molecular and pathways by the Ingenuity Pathway Analysis (IPA) database. Totally, 353 differentially expressed genes (DEGs) were identified, among which 181 genes were downregulated and 172 genes were upregulated in RPE\/choroid of AMD patients. Furthermore, several significantly enriched biological processes, including cancer, organismal injury and abnormalities, and ophthalmic disease, were identified associated with these DEGs. By analysis of canonical pathway, the phototransduction pathway and atherosclerosis signaling were the top two significant canonical pathways altered in RPE\/choroid tissues in human AMD. As expected, several ophthalmic disease-related molecules, including RHO, PDE6A, 3\u2032,5\u2032-cyclic-GMP phosphodiesterase, and G protein alpha, were in the central nodes of disease network. The bioinformatics technology combined with the existing high-throughput data was applied to evaluate the underlying key genes and pathways in human AMD tissues, which may predict downstream and upstream biological processes and identify potential therapeutic intervention targets in human AMD.<\/jats:p>","DOI":"10.1155\/2020\/2714746","type":"journal-article","created":{"date-parts":[[2020,8,21]],"date-time":"2020-08-21T23:31:28Z","timestamp":1598052688000},"page":"1-10","source":"Crossref","is-referenced-by-count":5,"title":["Identification of Key Genes and Pathways Associated with Age-Related Macular Degeneration"],"prefix":"10.1155","volume":"2020","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0239-6670","authenticated-orcid":true,"given":"Junyu","family":"Zhang","sequence":"first","affiliation":[{"name":"Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People\u2019s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu 611731, China"},{"name":"International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China"},{"name":"Department of Pathology, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1216-9893","authenticated-orcid":true,"given":"Yu","family":"Zhou","sequence":"additional","affiliation":[{"name":"Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People\u2019s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu 611731, China"},{"name":"Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People\u2019s Hospital, Chengdu 610072, China"},{"name":"Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA"},{"name":"Department of Genetics, 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