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Overexpression of ACE2 ameliorates Aβ‐induced blood–brain barrier damage and angiogenesis by inhibiting NF‐κB/VEGF/VEGFR2 pathway

Overexpression of ACE2 ameliorates Aβ‐induced blood–brain barrier damage and angiogenesis by... INTRODUCTIONAlzheimer's disease (AD) is the most common neurodegenerative disease, and its pathogenesis remains unclear.1 One of its primary pathological features is the extracellular deposition of β‐amyloid protein (Aβ), which can cause damage to the cerebrovascular system and the blood–brain barrier (BBB).2 Recent studies have demonstrated that cerebrovascular dysfunction, decreased cerebral blood flow, and BBB permeability impairment occur earlier than cognitive impairment.3 Therefore, improving vascular function may be significant for the progression and treatment of AD.Angiogenesis is the response of endothelial cells to hypoxia and inflammation, mediated by cytokine growth factors, which leads to the formation of a tubular network that enhances local microcirculation by bringing oxygen and nutrients to damaged tissues. Morphological and biochemical evidence of this process includes increased local capillary density, vascular ring formation, glomerular vascular structure formation, and expression of angiogenic factors such as vascular endothelial growth factor (VEGF), transforming growth factor, and tumor necrosis factor.4 The pathological anatomy results of postmortem AD patients showed that, compared with age‐matched healthy controls, AD patients had increased neovascularization, microvessels, and string vessels in the brain.5 String vessels are collapsed basement membranes without endothelial cells and have no function in circulation.6 Neovascularization in the AD brain is a response http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Animal Models and Experimental Medicine Wiley

Overexpression of ACE2 ameliorates Aβ‐induced blood–brain barrier damage and angiogenesis by inhibiting NF‐κB/VEGF/VEGFR2 pathway

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References (83)

Publisher
Wiley
Copyright
© 2023 The Chinese Association for Laboratory Animal Sciences.
eISSN
2576-2095
DOI
10.1002/ame2.12324
Publisher site
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Abstract

INTRODUCTIONAlzheimer's disease (AD) is the most common neurodegenerative disease, and its pathogenesis remains unclear.1 One of its primary pathological features is the extracellular deposition of β‐amyloid protein (Aβ), which can cause damage to the cerebrovascular system and the blood–brain barrier (BBB).2 Recent studies have demonstrated that cerebrovascular dysfunction, decreased cerebral blood flow, and BBB permeability impairment occur earlier than cognitive impairment.3 Therefore, improving vascular function may be significant for the progression and treatment of AD.Angiogenesis is the response of endothelial cells to hypoxia and inflammation, mediated by cytokine growth factors, which leads to the formation of a tubular network that enhances local microcirculation by bringing oxygen and nutrients to damaged tissues. Morphological and biochemical evidence of this process includes increased local capillary density, vascular ring formation, glomerular vascular structure formation, and expression of angiogenic factors such as vascular endothelial growth factor (VEGF), transforming growth factor, and tumor necrosis factor.4 The pathological anatomy results of postmortem AD patients showed that, compared with age‐matched healthy controls, AD patients had increased neovascularization, microvessels, and string vessels in the brain.5 String vessels are collapsed basement membranes without endothelial cells and have no function in circulation.6 Neovascularization in the AD brain is a response

Journal

Animal Models and Experimental Medicine – Wiley

Published: Jun 1, 2023

Keywords: ACE2; Alzheimer's disease; angiogenesis; blood–brain barrier; VEGF

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