Bloodretinal

Bloodretinal refers to the blood-retinal barrier (BRB), a selective interface that regulates exchanges between the bloodstream and retinal tissue. The BRB has two components: the inner BRB, formed by retinal microvascular endothelial cells sealed by tight junctions and supported by pericytes and glial endfeet; and the outer BRB, formed by the retinal pigment epithelium (RPE), whose tight junctions restrict passage between the choroidal circulation and the neural retina. Together, these barriers maintain retinal homeostasis and protect neural tissue from fluctuations in blood composition.

The BRB's primary function is to preserve the neural retina's specialized environment. It regulates ion and fluid balance, prevents the uncontrolled entry of plasma proteins, and enables selective transport of nutrients, gases, and waste. Transport occurs through paracellular routes regulated by tight junctions and through transcellular pathways carried by specific transporters. The barrier is dynamic and modulated by physiological and pathological signals, including vascular endothelial growth factor (VEGF) and inflammatory mediators.

Dysfunction of the BRB is central to many retinal diseases. Breakdown can lead to macular edema, retinal hemorrhages, and lipid exudates, contributing to vision loss. Diabetic retinopathy and retinal vein occlusions are among the most common conditions associated with BRB disruption, with VEGF-driven increases in permeability playing a key role. Diagnosis often involves fluorescein angiography to detect leakage and optical coherence tomography (OCT) to quantify edema.

Management focuses on reducing leakage and protecting retinal structure. Treatments include intravitreal anti-VEGF agents, corticosteroids, and laser therapies in selected cases, alongside systemic control of diabetes and hypertension. Ongoing research targets the molecular components of tight junctions, pericyte signaling, and the cellular interactions that maintain or restore BRB integrity.