Inner retinal ischaemia: current understanding and needs for further investigations

Abstract

. Inner retinal ischaemia is involved in the pathogenesis of major vision‐threatening diseases such as retinal vein thrombosis, diabetic retinopathy and retinopathy of prematurity. However, the pathogenesis of inner retinal ischaemia has not been fully elucidated, which represents an impediment to the development and improvement of techniques to prevent and treat these diseases on a rational basis. This paper provides a comprehensive review of current knowledge of the pathophysiology of inner retinal ischaemia, including clinical, anatomical and physiological aspects of disease development. It is suggested that chronic inner retinal ischaemia caused by capillary occlusion may develop secondary to an increase in hydrostatic pressure in the vessels. Further knowledge of the pathophysiology of inner retinal ischaemia can be obtained by identifying the mechanisms that lead to increased hydrostatic pressure in the capillary bed and establishing the structural and functional basis for the different response patterns in the central and peripheral areas of the retina that develop secondary to this increased hydrostatic pressure. Further elucidation of these unknown response patterns requires both in vitro and in vivo studies of retinal vascular pathophysiology. It is conceivable that a more detailed knowledge of these response patterns may help in the design of new treatments for retinal ischaemia and its vision‐threatening consequences.

Hypoxic retinal Müller cells promote vascular permeability by HIF-1–dependent up-regulation of angiopoietin-like 4

“…Mouse models, in which the hyperglycemic state is replicated, have proven essential for studying the early stages of diabetic eye disease. However, these models do not adequately reproduce the retinal nonperfusion that results in the release of growth factors that, in turn, promote the vascular permeability characteristic of patients with later stages of diabetic retinopathy (1). Although no animal model has yet been found to show all of the microvascular complications associated with patients with diabetic eye disease, the OIR mouse model faithfully reproduces the inner retina ischemia (nonperfusion) observed in patients with ischemic retinopathies, including the later stages of diabetic retinopathy; it has proven to be an important tool for studying the pathogenesis of these diseases (13).…”

“…diabetes | retinal vein occlusion | angiogenesis | transcription factor I schemic retinopathies include a diverse group of retinal diseases, in which immature retinal vasculature (e.g., retinopathy of prematurity or incontinentia pigmenti) or damage to mature retinal vessels (e.g., diabetic retinopathy, retinal vein occlusion, or sickle cell retinopathy) leads to retinal ischemia (1). Although diverse (and poorly understood) etiologies may lead to insufficient perfusion of the retina, all lead to a common sequelae: the formation of abnormal leaky blood vessels that can manifest clinically with the accumulation of fluid in the inner retina [i.e., macular edema (ME)] and often, a profound loss of vision (2).…”

The Effect of Neovascularization on Human Retinal Pigment Epithelium after Hyperbaric Oxygen Therapy

“…In diseases such as diabetic retinopathy, branched retinal vein occlusion or retinopathy of prematurity, the retinal tissue develops pathological changes after experiencing tissue ischemia. Ischemia develops when the blood supply is inadequately provided to allow sufficient amount of oxygen and nutrients for proper cell functioning [20]. Ischemia deprives tissues of three survival requirements: oxygen, metabolic substrates and removal of waste products.…”

Interleukin-33 Prevents Retinal Ischemia Reperfusion Injury in Rats by Preventing Apoptosis

“…RIR injury is a common clinical condition that occurs in a variety of ocular pathologies, including retinal vascular occlusion, acute glaucoma, diabetic retinopathy, and ophthalmic operations that affect the retinal blood flow, and which represents the main cause of irreversible vision loss in humans (17). The pathogenesis of RIR injury is complicated and is not completely understood.…”