Retinal astrocytes reside mainly in the nerve fiber layer and are central to shaping retinal vessels and maintaining neurovascular balance. Derived from the optic nerve head, they spread across the inner retina to form a meshwork that both supports and instructs the emerging superficial vascular plexus. Immature astrocytes supply vascular endothelial growth factor-A(VEGF-A) to guide endothelial sprouting, while signals from growing vessels promote astrocyte maturation and strengthen the blood–retinal barrier. In disorders such as diabetic retinopathy and neovascular age-related macular degeneration, these cells show marked plasticity. Reactive astrogliosis can sustain VEGF and inflammation, favoring fragile, leaky neovessels, whereas alternative astrocyte states help reinforce barrier function and release anti-angiogenic factors. Located at the core of the neurovascular unit, astrocytes communicate continuously with endothelial cells, pericytes and neurons. This review integrates data from single-cell profiling and advanced imaging to outline astrocyte development, morphology and key signaling pathways (VEGF, PDGF, Wnt/Norrin, Eph/ephrin), and considers how tuning astrocyte polarization might be exploited to preserve retinal vascular integrity.

Purpose: To investigate the impact of anti–vascular endothelial growth factor therapy on epiretinal macrophage-like cells (eMLC) in branch retinal vein occlusion with macular edema (BRVO-ME) patients. Methods: This retrospective study included 58 BRVO-ME patients treated with anti–vascular endothelial growth factor agents, divided into 2 groups: 28 eyes (1–2 Injection group) and 30 eyes (3 Injection group). The 3-injection group comprised 20 early responders and 10 limited early responders (LERs). Longitudinal changes in macular eMLC count and density were assessed through en face optical coherence tomography during the early response phase (baseline to 3 months postinitial injection). Linear regression and Spearman correlation analyzed eMLC density's relationship with optical coherence tomography angiography parameters and systemic inflammatory indices. Results: The 3-injection group exhibited greater reductions in macular edema and eMLC density than the 1 to 2 injection group. Macular eMLC density significantly decreased in early responders, whereas LERs showed no significant alteration. Posttreatment central macular thickness change positively correlated with eMLC density change (r = 0.57). Baseline systemic inflammatory indices (neutrophil/lymphocyte ratio, r = −0.46; neutrophil/platelet ratio, r = −0.36; systemic immune-inflammation index, r = −0.33; systemic inflammatory response index, r = −0.31) negatively correlated with posttreatment eMLC density change. Conclusion: Anti–vascular endothelial growth factor therapy reduces macular eMLC in BRVO-ME patients, especially in early responders receiving three injections. Macular eMLCs are closely associated with inflammation and may serve as a valuable treatment response biomarker.