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Review
. 2010;224 Suppl 1(Suppl 1):16-24.
doi: 10.1159/000315152. Epub 2010 Aug 18.

The Multifactorial Nature of Retinal Vascular Disease

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Free PMC article
Review

The Multifactorial Nature of Retinal Vascular Disease

Mark E Kleinman et al. Ophthalmologica. .
Free PMC article

Abstract

Retinal vascular disease is the most common cause of macular edema (ME). While there are several etiologies of vascular compromise and subsequent macular leakage, diabetic retinopathy is the most prevalent and continues to challenge ophthalmologists and frustrate patients due to its refractory nature. In response to this epidemic, diabetic ME (DME) along with cystoid ME (CME) have been areas of active investigation both in the clinic and the laboratory. Several decades of basic science research have revealed a growing and complex array of cytokine growth factors and proinflammatory mediators which are capable of inciting the cellular changes that result in accumulation of fluid within the retina. Much of this new molecular foundation provides the current and fundamental scaffold for understanding the pathologic process of ME while simultaneously identifying potential therapeutic targets. Whereas CME has classically been treated with corticosteroids and nonsteroidal antiinflammatory drugs, recent clinical studies have demonstrated improved visual outcomes for DME treatment with light focal/grid laser, corticosteroids and anti-vascular endothelial growth factor antibodies. Yet, each of these treatments has differential effects on the multifactorial mechanisms of ME. This article reviews the anatomical, cellular and molecular derangements associated with ME and highlights specific pathways targeted by current treatments.

Figures

Fig. 1
Fig. 1
Molecular pathways of inflammation via AA formation and downstream induction of cyclooxygenases and 5-lipoxygenase which generate PG and leukotrienes, respectively. While aspirin (ASA) and nonsteroidal antiinflammatory drugs (NSAID) inhibit PG, prostacyclin and thromboxane synthesis, corticosteroids act further upstream via inhibition of PLA2, which prevents the release of AA and activation of multiple downstream inflammatory cascades. Zileuton is a targeted 5-lipoxygenase antagonist.
Fig. 2
Fig. 2
Corticosteroids have a multipronged effect in vivo, leading to the suppression of several proinflammatory mechanisms.

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