Overexpression of ACE2 ameliorates Aβ-induced blood-brain barrier damage and angiogenesis by inhibiting NF-κB/VEGF/VEGFR2 pathway.
Xueling ZhangYu ZhangLing ZhangChuan QinPublished in: Animal models and experimental medicine (2023)
Overexpression of ACE2 can improve pathological angiogenesis and blood-brain barrier damage in AD models in vitro by inhibiting NF-κB/VEGF/VEGFR2 pathway activity. ACE2 may therefore represent a therapeutic target for endothelial cell dysfunction in AD.
Keyphrases
- blood brain barrier
- vascular endothelial growth factor
- endothelial cells
- signaling pathway
- high glucose
- oxidative stress
- angiotensin converting enzyme
- angiotensin ii
- diabetic rats
- pi k akt
- lps induced
- cell proliferation
- cerebral ischemia
- transcription factor
- nuclear factor
- mouse model
- immune response
- inflammatory response
- toll like receptor