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Pathophysiology of Diabetic Macular Edema

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Diabetic Macular Edema

Abstract

The unique structural organization of the retinal microvasculature is essential for the healthy maintenance of the retina. Primarily responsible for the regulation of vascular permeability within this tissue, the blood–retinal barrier (BRB) is a physiological barrier essential for normal visual function. Tightly regulating fluid and electrolyte balance in the surrounding tissue, the BRB is formed by the interaction between specialized cells and the underlying basement membrane. In diabetes, the hyperglycemic environment causes the alteration of this barrier. Unable to regulate vascular permeability, the breakdown of the BRB leads to the leakage of plasma and lipids into the retina, the clinical manifestation of diabetic macular edema (DME). In this chapter, we discuss the key players (VEGF and molecules beyond VEGF) involved in the maintenance of this barrier and the molecular mechanisms that lead to its breakdown. Known to be involved in this disease, we highlight the role of inflammation in DME. Current available therapies have limitations; thus, we point to the various pro-inflammatory mediators involved and discuss their therapeutic potential in the treatment of DME.

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Acknowledgments

The work reported in this chapter was supported by the National Institutes of Health under award number NIH R01 EY 028606-01-A1 and VA Merit Review award number 1I01BX005348-01A1.

None of the authors have any financial/conflicting interests to disclose.

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Cabrera, A.P., Wolinsky, E.L., Mankad, R.N., Monickaraj, F., Das, A. (2022). Pathophysiology of Diabetic Macular Edema. In: Saxena, S., Cheung, G., Lai, T.Y., Sadda, S.R. (eds) Diabetic Macular Edema. Springer, Singapore. https://doi.org/10.1007/978-981-19-7307-9_2

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