Vincenzo Starace, Marco Battista, Maria Brambati, Michele Cavalleri, Federico Bertuzzi, Alessia Amato, Rosangela Lattanzio, Francesco Bandello, Maria Vittoria Cicinelli
{"title":"The role of inflammation and neurodegeneration in diabetic macular edema.","authors":"Vincenzo Starace, Marco Battista, Maria Brambati, Michele Cavalleri, Federico Bertuzzi, Alessia Amato, Rosangela Lattanzio, Francesco Bandello, Maria Vittoria Cicinelli","doi":"10.1177/25158414211055963","DOIUrl":null,"url":null,"abstract":"<p><p>The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.</p>","PeriodicalId":23054,"journal":{"name":"Therapeutic Advances in Ophthalmology","volume":null,"pages":null},"PeriodicalIF":2.3000,"publicationDate":"2021-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2a/8c/10.1177_25158414211055963.PMC8652911.pdf","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Therapeutic Advances in Ophthalmology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/25158414211055963","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"OPHTHALMOLOGY","Score":null,"Total":0}
引用次数: 12
Abstract
The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.