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Diabetic retinopathy (DR) is the leading cause of vision loss among working age population worldwide. Due to numerous advances in the modern medicine, substantial progress has been made in the treatment of DR. The central role of vascular endothelial growth factor (VEGF) in the pathogenesis of DR was validated by the finding that the higher concentrations of VEGF-A in vitreous correlate positively with the more advanced stages of DR and diabetic macular edema (DME).1 The studies on diabetic animal models and clinical practice demonstrated that the VEGF-A blockade is effective to treat proliferative diabetic retinopathy (PDR) and DME and even to halt the progression or reverse the stages of moderate-to-severe noneproliferative diabetic retinopathy (NPDR).2 Hence, ophthalmologists learnt from oncologists and adapted anti-VEGF therapy to counterattack VEGFdriven etiology of DR. The anti-VEGF therapy has revolutionized DR treatment. However, a significant subset of patients with DME and PDR failed to respond to anti-VEGF therapy.3 Nevertheless, the strategies for prevention and management of early DR are still lacking. Therefore, there is an urgent need for the discovery of new therapeutic targets for managing DR. This book tries to update the basic understanding of aberrant metabolisms induced by diabetes mellitus, by which the homeostasis of retinal neurovascular unit (NVU) is disturbed in DR. The diabetes-induced disturbed retinal neurovascular coupling among neurons, glia, and vascular cells results in key pathogenic events of DR. These pathogenic events include hyperglycemia-induced oxidative stress, apoptosis, microinflammation, blooderetinal barrier breakdown, and pathological angiogenesis. Based on the new understanding of these pathogenic mechanisms, the aim of this book is to explore how these research achievements can be translated into current and future clinical applications from physician’s and researcher’s perspective. This book emphasizes how several novel pathobiological concepts of DR have been translated into potential therapeutic targets. First of all, DR is a complication of diabetes. Most advances in systemic treatment of diabetes have been related to secondary prevention of DR. Second, DR is defined as a disease of NVU, comprising both neurodegeneration and microangiopathy. The interplay between these two components in retinal NVU determines that the therapeutic strategy must cover both. Third, the development and progression of DR are disease stage specific.4 The anatomically regressive stage of DR, such as dynamic nonperfused retina, is due to vascular and neuronal apoptosis. In this stage antiapoptotic, protective therapy is essential, while the proliferative stage of DR is based on pathologic angiogenesis. Therefore, targeting VEGF and non-VEGF pathways to suppress angiogenesis is imperative. Fourth, DR refers to a disease of microinflammation. Abnormal activation of glia and inflammatory cells and the imbalance of pro- and antiinflammatory cytokines contribute to and aggravate different stages of DR. Thereby, antiinflammatory therapy is gaining ground in treating DR, particularly for DME in years to come. Fifth, this book tries to point out how the advances of multimodal imaging techniques and artificial intelligence-directed medicine have been translated from bench to bedside. Lastly, we expect that the rapidly improving retinal microsurgery will bring promise for patients with late stage of PDR. Although this book has emphasized the translational approach, the current evidence-based DR management is still introduced in the highest priority, followed by therapies in pipeline for DR. In a sequential order, the potential mechanism-based therapies are discussed at the end of each chapter. The study of “therapeutic targets for DR” from molecule to system is far ranging, which is beyond the scope of this book. We humbly present this book to readers, to make some initial remarks to set the ball rolling for future breakthroughs.