{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:32:12Z","timestamp":1790699532512,"version":"4.1.0"},"reference-count":178,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2016,9,7]],"date-time":"2016-09-07T00:00:00Z","timestamp":1473206400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Diabetic retinopathy is the leading cause of blindness in working age adults, and is projected to be a significant future health concern due to the rising incidence of diabetes. The recent advent of anti-vascular endothelial growth factor (VEGF) antibodies has revolutionized the treatment of diabetic retinopathy but a significant subset of patients fail to respond to treatment. Accumulating evidence indicates that inflammatory cytokines and chemokines other than VEGF may contribute to the disease process. The current review examines the presence of non-VEGF cytokines in the eyes of patients with diabetic retinopathy and highlights mechanistic pathways in relevant animal models. Finally, novel drug targets including components of the kinin\u2013kallikrein system and emerging treatments such as anti-HPTP (human protein tyrosine phosphatase) \u03b2 antibodies are discussed. Recognition of non-VEGF contributions to disease pathogenesis may lead to novel therapeutics to enhance existing treatments for patients who do not respond to anti-VEGF therapies.<\/jats:p>","DOI":"10.3390\/ijms17091498","type":"journal-article","created":{"date-parts":[[2016,9,7]],"date-time":"2016-09-07T09:59:46Z","timestamp":1473242386000},"page":"1498","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":94,"title":["Moving Past Anti-VEGF: Novel Therapies for Treating Diabetic Retinopathy"],"prefix":"10.3390","volume":"17","author":[{"given":"Mark","family":"Bolinger","sequence":"first","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, Kellogg Eye Center, and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48105, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Antonetti","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, Kellogg Eye Center, and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48105, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2016,9,7]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"s84","DOI":"10.2337\/diacare.26.1.226","article-title":"Retinopathy in Diabetes","volume":"26","author":"Fong","year":"2003","journal-title":"Diabetes Care"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"143","DOI":"10.2337\/diacare.21.1.143","article-title":"Diabetic retinopathy","volume":"21","author":"Aiello","year":"1998","journal-title":"Diabetes Care"},{"key":"ref_3","unstructured":"Centers for Disease Control and Prevention (1996). 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