Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction

Abstract

Endothelial dysfunction (ED) is a core pathophysiological process. The abnormal response of vascular endothelial (VE) cells to risk factors can lead to systemic consequences. ED caused by intermittent hypoxia (IH) has also been recognized. Neuropeptide Y (NPY) is an important peripheral neurotransmitter that binds to different receptors on endothelial cells, thereby causing ED. Additionally, hypoxia can induce the release of peripheral NPY; however, the involvement of NPY and its receptor in IH-induced ED has not been determined. This review explains the definition of chronic IH and VE function, including the relationship between ED and chronic IH-related vascular diseases. The results showed that that the effect of IH on VE injury is mediated by the VE-barrier structure and endothelial cell dysfunction. These findings offer new ideas for the prevention and treatment of obstructive sleep apnea syndrome and its complications.

Ginsenoside Rg1 ameliorates chronic intermittent hypoxia-induced vascular endothelial dysfunction by suppressing the formation of mitochondrial reactive oxygen species through the calpain-1 pathway

“…The imbalance between oxidizing and antioxidant defense systems contributes to the activation of oxidative stress, which is manifested as enhanced levels of ROS and MDA, causing endothelial activation and eventually leading to VED [ 32 , 33 ]. The occurrence of VED facilitates increased vascular resistance, leading to vascular diseases, including coronary artery disease, cerebrovascular disease and peripheral artery disease [ 3 , 34 , 35 ]. In our study, ginsenoside Rg1 treatment reversed the downregulated mitochondrial membrane potential in HCAECs and the upregulated level of mitoROS in aortas and HCAECs exposed to CIH.…”

Protective effect of Astragaloside IV on chronic intermittent hypoxia-induced vascular endothelial dysfunction through the calpain-1/SIRT1/AMPK signaling pathway

“…The model of CIH exposure established in this study was reported previously ( Jiang et al, 2020 ). Briefly, the mice were exposed to cages of automated, computer-controlled O 2 concentration exchange systems (Proox-100, Shanghai Tow-Int Tech Ltd.) to achieve a similar oxyhemoglobin saturation (SpO 2 ) nadir (50∼60%) in moderate to severe patients based on previous studies ( Zhou et al, 2014 ; Hu et al, 2021 ; Li et al, 2021 ). The mice were exposed to 20 hypoxic events/h (90 s of 21% O 2 and 90 s of 10% O 2 ) for 8 h/day for 4 weeks.…”

Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?

“…Several studies suggest that hypoxia causes structural and functional alterations in the brain endothelium via different mechanisms, including rearrangement of the endothelial cytoskeleton, altering intercellular adhesions of endothelial cells, and promoting endothelial constriction, apoptosis, and degeneration [141]. Studies of intermittent hypoxia suggest that endothelial cell resistance is reduced due to ROS-dependent activation of the extracellular signal-regulated kinase (ERK1/2) pathway and c-Jun N-terminal kinase (JNK)-mediated re-arrangement of the endothelial cytoskeleton, including the redistribution of actin stress fibers and VE-cadherin, leading to abnormal endothelial barrier function [142,143].…”