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The role of inflammation in diabetic eye disease

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Abstract

Mounting evidence suggests that immunological mechanisms play a fundamental role in the pathogenesis of diabetic retinopathy (DR) and diabetic macular edema (DME). Upregulation of cytokines and other proinflammatory mediators leading to persistent low-grade inflammation is believed to actively contribute to the DR-associated damage to the retinal vasculature, inducing breakdown of the blood-retinal barrier, subsequent macular edema formation, and promotion of retinal neovascularization. This review summarizes the current knowledge of the biological processes providing an inflammatory basis for DR and DME. In addition, emerging therapeutic approaches targeting inflammation are discussed, including blockade of angiopoietin 2 and other molecular targets such as interleukin (IL)-6, IL-1β, plasma kallikrein, and integrins.

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Abbreviations

AGEs:

advanced glycation end products

BRB:

blood-retinal barrier

DME:

diabetic macular edema

NPDR:

nonproliferative diabetic retinopathy

PDR:

proliferative diabetic retinopathy

VEGF:

vascular endothelial growth factor

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Acknowledgments

The authors would like to thank Jayashree Sahni, Meike Pauly-Evers, and Robert Weikert for the BOULEVARD study data and manuscript review.

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Correspondence to Marina Mesquida.

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MM, FD, and SF are employed by F. Hoffmann-La Roche Ltd., Basel, Switzerland.

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This article is a contribution to the special issue on Inflammation and Type 2 Diabetes - Guest Editor: Marc Y. Donath

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Mesquida, M., Drawnel, F. & Fauser, S. The role of inflammation in diabetic eye disease. Semin Immunopathol 41, 427–445 (2019). https://doi.org/10.1007/s00281-019-00750-7

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