Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis

Cardiovascular disease is the leading cause of death worldwide. Endothelial dysfunction of the arterial vasculature plays a pivotal role in cardiovascular pathogenesis. Nicotine-induced endothelial dysfunction substantially contributes to the development of arteriosclerotic cardiovascular disease. N...

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Main Authors: Yan-li Zheng, Wan-da Wang, Mei-mei Li, Shu Lin, Hui-li Lin
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-02-01
Series:Frontiers in Cardiovascular Medicine
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcvm.2021.630968/full
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author Yan-li Zheng
Wan-da Wang
Mei-mei Li
Shu Lin
Shu Lin
Shu Lin
Hui-li Lin
author_facet Yan-li Zheng
Wan-da Wang
Mei-mei Li
Shu Lin
Shu Lin
Shu Lin
Hui-li Lin
author_sort Yan-li Zheng
collection DOAJ
description Cardiovascular disease is the leading cause of death worldwide. Endothelial dysfunction of the arterial vasculature plays a pivotal role in cardiovascular pathogenesis. Nicotine-induced endothelial dysfunction substantially contributes to the development of arteriosclerotic cardiovascular disease. Nicotine promotes oxidative inflammation, thrombosis, pathological angiogenesis, and vasoconstriction, and induces insulin resistance. However, the exact mechanism through which nicotine induces endothelial dysfunction remains unclear. Neuropeptide Y (NPY) is widely distributed in the central nervous system and peripheral tissues, and it participates in the pathogenesis of atherosclerosis by regulating vasoconstriction, energy metabolism, local plaque inflammatory response, activation and aggregation of platelets, and stress and anxiety-related emotion. Nicotine can increase the expression of NPY, suggesting that NPY is involved in nicotine-induced endothelial dysfunction. Herein, we present an updated review of the possible mechanisms of nicotine-induced atherosclerosis, with a focus on endothelial cell dysfunction associated with nicotine and NPY.
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spelling doaj.art-46669fccd7234644a8c731816f2ead1b2022-12-21T22:00:18ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2021-02-01810.3389/fcvm.2021.630968630968Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and AtherosclerosisYan-li Zheng0Wan-da Wang1Mei-mei Li2Shu Lin3Shu Lin4Shu Lin5Hui-li Lin6Department of Cardiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaDepartment of Cardiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaCentre of Neurological and Metabolic Research, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaDiabetes and Metabolism Division, Garvan Institute of Medical Research, Sydney, NSW, AustraliaDepartment of Cardiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, ChinaCardiovascular disease is the leading cause of death worldwide. Endothelial dysfunction of the arterial vasculature plays a pivotal role in cardiovascular pathogenesis. Nicotine-induced endothelial dysfunction substantially contributes to the development of arteriosclerotic cardiovascular disease. Nicotine promotes oxidative inflammation, thrombosis, pathological angiogenesis, and vasoconstriction, and induces insulin resistance. However, the exact mechanism through which nicotine induces endothelial dysfunction remains unclear. Neuropeptide Y (NPY) is widely distributed in the central nervous system and peripheral tissues, and it participates in the pathogenesis of atherosclerosis by regulating vasoconstriction, energy metabolism, local plaque inflammatory response, activation and aggregation of platelets, and stress and anxiety-related emotion. Nicotine can increase the expression of NPY, suggesting that NPY is involved in nicotine-induced endothelial dysfunction. Herein, we present an updated review of the possible mechanisms of nicotine-induced atherosclerosis, with a focus on endothelial cell dysfunction associated with nicotine and NPY.https://www.frontiersin.org/articles/10.3389/fcvm.2021.630968/fullneuropeptide Ynicotineendothelial dysfunctionatherosclerosiscardiovascular disease
spellingShingle Yan-li Zheng
Wan-da Wang
Mei-mei Li
Shu Lin
Shu Lin
Shu Lin
Hui-li Lin
Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis
Frontiers in Cardiovascular Medicine
neuropeptide Y
nicotine
endothelial dysfunction
atherosclerosis
cardiovascular disease
title Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis
title_full Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis
title_fullStr Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis
title_full_unstemmed Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis
title_short Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis
title_sort updated role of neuropeptide y in nicotine induced endothelial dysfunction and atherosclerosis
topic neuropeptide Y
nicotine
endothelial dysfunction
atherosclerosis
cardiovascular disease
url https://www.frontiersin.org/articles/10.3389/fcvm.2021.630968/full
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