الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Diabetic macular edema is a major cause of visual impairment worldwide. Past research didn’t reach for the exact pathophysiology of diabetic macular edema (DME), which revealed to be complex and almost multifactorial pathways are involved. Many structural and cellular changes prevail. Structural and cellular changes involve neurovascular unit (NVU) (microangiopathy, neuronal tissue and various glial tissue), inner and outer blood retinal barrier (BRB), inflammatory process, and finally various types of cell death. Molecular changes comprise intracellular pathological changes that affects many known and unknown pathways, of note: polyol pathway, advanced glycation end-products (AGEs) precursor formation, Protein kinase C (PKC) pathway and finally Hexosamine pathway among several others.
Several attempts throughout decades were done seeking treatment. Macular grid laser, intravitreal injection of corticosteroids and finally anti-vascular endothelial growth factors (anti-VEGFs) were the available solutions. With different grades of effect and superiority of anti-VEGFS, unfortunately, they all failed to achieve complete success.