Silencing Nogo-B improves the integrity of blood-retinal barrier in diabetic retinopathy via regulating Src, PI3K/Akt and ERK pathways

2021 ◽  
Vol 581 ◽  
pp. 96-102
Author(s):  
Qian Yang ◽  
Chaoyang Zhang ◽  
Hai Xie ◽  
Lei Tang ◽  
Dandan Liu ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Blood Retinal Barrier

Mechanistic Insights into Immunological Therapy for Targeting Diabetic Retinopathy

2021 ◽  
Vol 5 (3) ◽  
pp. 01-05
Author(s):  
Imteyaz Qamar
Keyword(s):  
Diabetic Retinopathy ◽  
Progressive Disease ◽  
Common Complication ◽  
Blood Retinal Barrier ◽  
Immunological Therapy ◽  
Tnf Α ◽  
Capillary Occlusion ◽  
Inflammatory Molecules ◽  
Inflammatory Effect

Diabetic retinopathy (DR) is a common complication amongst patients that have diabetes. It is a leading cause of blindness in middle age people. A large proportion of patients who have diabetes develop retinopathy. There are several immunological reasons associated with the pathophysiology of this disease. Role of several mediators that increase the oxidative stress and have a pro-inflammatory effect which leads to capillary occlusion and neovascularization (NV). Increased vasopermeability due to disruption of the blood-retinal barrier (BRB) leading to diabetic macular edema (DME). Immunotherapies utilise different compounds and target various inflammatory molecules like TNF-α and pathways such as PPARγ for treatment of this progressive disease. Inflammatory and pro-inflammatory pathways are found to have an essential role in promoting DR; therefore, targeting them provides a useful technique for curing DR.

Erythropoietin protects outer blood‐retinal barrier in experimental diabetic retinopathy by up‐regulating ZO‐1 and occludin

2019 ◽  
Vol 47 (9) ◽  
pp. 1182-1197 ◽  
Author(s):  
Chaoyang Zhang ◽  
Hai Xie ◽  
Qian Yang ◽  
Yiting Yang ◽  
Weiye Li ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Blood Retinal Barrier

scholarly journals A Potential Role for Angiopoietin 2 in the Regulation of the Blood–Retinal Barrier in Diabetic Retinopathy

2011 ◽  
Vol 52 (6) ◽  
pp. 3784 ◽  
Author(s):  
Sampathkumar Rangasamy ◽  
Ramprasad Srinivasan ◽  
Joann Maestas ◽  
Paul G. McGuire ◽  
Arup Das
Keyword(s):  
Diabetic Retinopathy ◽  
Potential Role ◽  
Blood Retinal Barrier ◽  
Angiopoietin 2

scholarly journals Erythropoietin protects the inner blood–retinal barrier by inhibiting microglia phagocytosis via Src/Akt/cofilin signalling in experimental diabetic retinopathy

Diabetologia ◽  
2020 ◽  
Vol 64 (1) ◽  
pp. 211-225
Author(s):  
Hai Xie ◽  
Chaoyang Zhang ◽  
Dandan Liu ◽  
Qian Yang ◽  
Lei Tang ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Blood Retinal Barrier

The Blood–Retinal Barrier in Retinal Disease

2009 ◽  
Vol 03 (02) ◽  
pp. 105 ◽  
Author(s):  
José Cunha-Vaz ◽  
Keyword(s):  
Diabetic Retinopathy ◽  
Tight Junctions ◽  
Retinal Pigment ◽  
Water Flux ◽  
Retinal Disease ◽  
Retinal Pigment Epithelial Cells ◽  
Age Related Macular Degeneration ◽  
Retinal Diseases ◽  
Blood Retinal Barrier ◽  
Age Related

The blood–ocular barrier system is formed by two main barriers: the blood–aqueous barrier and the blood–retinal barrier (BRB). The BRB is particularly tight and restrictive and is a physiological barrier that regulates ion, protein and water flux into and out of the retina. The BRB consists of inner and outer components, the inner BRB being formed of tight junctions between retinal capillary endothelial cells and the outer BRB of tight junctions between retinal pigment epithelial cells. The BRB is essential to maintaining the eye as a privileged site and is essential for normal visual function. Alterations of the BRB play a crucial role in the development of retinal diseases. The two most frequent and relevant retinal diseases, diabetic retinopathy and age-related macular degeneration (AMD), are directly associated with alterations of the BRB. Diabetic retinopathy is initiated by an alteration of the inner BRB and neovascular AMD is a result of an alteration of the outer BRB. Treatment of retinal diseases must also deal with the BRB either by using its specific transport mechanisms or by circumventing it through intravitreal injections

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