The landmark publications that gave such impetus to our understanding of proliferative diabetic retinopathy are reviewed in the light of more recent reports. Briefly, confluence of small areas of capillary closure in the midperipheral and peripheral retina results in arteriovenous shunting and abnormal oxygen partial pressure gradients. These gradients embrace a chronic ischaemic penumbra that stimulates neuroglial secretion of angiogenic growth factors and upregulation of their receptors in the retinal venous endothelium and adventitia. The blood shunting produces biomechanical stresses within the veins and induces microvascular intussusception near arteriovenous crossings, giving way to neovascular outgrowths and/or segmental venous lesions (such as omega loops and coils) that penetrate the inner limiting lamina. The lamellar collagenous matrix of the vitreous cortex is then exploited for integrin‐dependent rete expansion along chemotactic gradients. During posterior vitreous detachment, haemorrhaging takes place from the arterialised veins as venous neovascular peduncles are avulsed.
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