Abstract
Diabetic retinopathy (DR), the most common cause of vision loss in diabetes, is characterized by vascular and neuronal abnormalities of the retina. As the main glial cells of the retina, Müller cells (MCs) are essential to the homeostasis and functionality of the retina. According to recent studies, MCs exhibit morphological and functional alterations, triggering the disease’s progression in DR. Retinal damage becomes exacerbated by their contribution in neurovascular unit disruption, pro-inflammatory cytokine release, and oxidative stress. Additionally, abnormal reactivity of these cells to high glucose circumstances compromises the health of neurons by causing glutamate accumulation and reducing potassium buffering. Comprehending the diverse functions of MCs in DR could facilitate the development of focused treatments aiming at slowing down the progression of the illness.