The role of plasmalemma vesicle-associated protein in pathological breakdown of blood-brain and blood-retinal barriers: potential novel therapeutic target for cerebral edema and diabetic macular edema

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diabetic retinopathy 7 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases

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diabetic retinopathy 1952 pathological conditions associated with a compromised barrier function such as cancer, ischemic stroke and diabetic retinopathy . Here, we discuss the current understanding of PLVAP as a structural component of endothelial cells
diabetic retinopathy 2794 occurs in pathological conditions such as trauma, acute ischemic stroke [[1]], brain tumors [[2]] and diabetic retinopathy [[3]], causes leakage of fluid and plasma proteins from the vasculature into the surrounding tissue
diabetic retinopathy 10315 under pathological conditions associated with barrier disruption such as brain ischemia, cancer and diabetic retinopathy [[22], [23], [25], [35]–[38]]. Notably, expression of the PAL-E antigen in retinal vessels positively
diabetic retinopathy 24706 conditions, whereas VEGFR2 and VEGFR3 are also highly expressed in pathological conditions such as diabetic retinopathy [[74], [75]]. Several studies demonstrate that VEGF positively regulates PLVAP expression. For instance,
diabetic retinopathy 42174 expression in the BBB and BRB is induced in pathological conditions associated with vascular leakage such as diabetic retinopathy [[25], [37], [75]], brain ischemia [[35], [36]] and brain tumors [[22], [23], [35]]. Collectively, these
diabetic retinopathy 47558 retinal vessels [[74], [75]], mediate vascular leakage (not shown). b In pathological conditions such as diabetic retinopathy , tissue VEGF-A levels are high. In addition, VEGFR2 and VEGFR3 are highly expressed in retinal vessels
diabetic retinopathy 56515 for conditions associated with angiogenesis such as age-related macular degeneration, proliferative diabetic retinopathy and cancer.Therapeutic perspective: targeted drug delivery via caveolaeBesides the potential to restore
hyperglycemia 53012 other arterial thrombo-embolic events [[111], [112]].Apart from the management of risk factors such as hyperglycemia and hypertension [[113]], current treatment options for DME consist of anti-VEGF agents, corticosteroids
hypertriglyceridemia 22582 which survive up to 3–4 months and suffer from growth retardation, edema, severe hypoproteinemia and hypertriglyceridemia [[57]].Together, these results show that PLVAP plays a crucial role during the development of the cardiovascular

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