Jakob Körbelin

This study identifies miR-23b as a negative regulator of BBB integrity and shows that anti-miR-23b enhances barrier function through multiple signaling pathways and improves outcomes in a stroke model.

This study shows that reducing Serpine1 in endothelial cells after stroke improves recovery by reducing blood flow and preventing blood-brain barrier damage.

This study shows that enhancing CD73 in mouse brain endothelial cells reduces infarct volume and mortality after stroke by promoting adenosine production and modulating neuroinflammation.

This paper identifies JUNB as a key driver of chronic brain vascular inflammation in CCM disease through multi-omic analysis of endothelial cell activation.

The paper shows that angiogenesis in the adult mouse cortex is regionally specific and Notch1 dependent, with increased angiogenesis in posterior-lateral regions upon Notch1 knockdown.

This study shows IL-10 signalling contributes to capillary stalling and cognitive impairment in type 1 diabetes by increasing vascular obstructions and reducing blood flow.

AAV-BR1-NPC2 gene therapy reduces cholesterol deposition and neurological symptoms in NP-C2 mice by delivering NPC2 to brain endothelial cells and neurons.

The paper shows high shear stress induces endothelial-mesenchymal transition and pulmonary arterial hypertension by reducing ERG expression, which can be mitigated by ERG replenishment.

This study demonstrates that gene therapy targeting brain endothelial cells improves neurological symptoms in a mouse model of MCT8 deficiency by increasing brain T3 levels and motor function.

The paper uses AAV-BR1 to target endothelial cells in the mouse retina, identify their morphology, and deliver Cx43 for studying microvascular function.

This study shows that CD2AP loss in brain endothelial cells impairs vascular function and memory in AD models, suggesting therapeutic targeting of CD2AP pathways.

This study shows that blood vessel regression in the brain reduces neuronal activity by impairing mitochondrial metabolism and glutamate production.