Abstract: Ischemic retinopathy is a leading cause of blindness: Ischemic retinopathies including diabetic retinopathy (DR), retinopathy of prematurity, and retinal artery and vein occlusion are major causes of visual impairment. Ischemic retinopathy can be acute, such as in central or branch retinal artery occlusion, or chronic, such as with DR (Figure 1). Although the causes of retinopathies are diverse, one pathogenic event shared by these conditions is the myeloid cell response to retinal ischemia (Shahror et al., 2024a). The ischemia-induced neurovascular injury results in progressive cell death by apoptosis, causing neurodegeneration and loss of vascular cells. Concurrently, there is activation and proliferation of microglia, non-parenchymal macrophages (such as perivascular macrophages), and recruitment of blood-borne (infiltrating) monocytes. These activated cells (collectively termed “myeloid cells”) play either a protective or deleterious role after retinal injury depending on their molecular profile and activation state. Our publications and others recently introduced the concept that myeloid cells (microglia and macrophages) can be geared to a pro-resolving phenotype to protect the retina against injury (Shahror et al., 2024a). This protective effect can be conferred by the secretion of reparative cytokines. Moreover, the direct interaction of myeloid cells with dead cells in the inner retina following ischemic injury has been described in retinal ischemia-reperfusion injury, suggesting microglia/macrophage-mediated phagocytic clearance of dead cells or efferocytosis (Abcouwer et al., 2021).