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Current views on neuropeptide Y and diabetes-related atherosclerosis

Abstract

Diabetes-induced atherosclerotic cardiovascular disease is the leading cause of death of diabetic patients. Neuronal regulation plays a critical role in glucose metabolism and cardiovascular function under physiological and pathological conditions, among which, neurotransmitter neuropeptide Y has been shown to be closely involved in these two processes. Elevated central neuropeptide Y level promotes food intake and reduces energy expenditure, thereby increasing adiposity. Neuropeptide Y is co-localized with noradrenaline in central and sympathetic nervous systems. As a major peripheral vascular contractive neurotransmitter, through interactions with its receptors, neuropeptide Y has been implicated in the pathology and progression of diabetes, by promoting the proliferation of endothelial cells and vascular fibrosis, which may contribute to diabetes-induced cardiovascular disease. Neuropeptide Y also participates in the pathogenesis of atherosclerosis, the major form of cardiovascular disease, via aggravating endothelial dysfunction, growth of vascular smooth muscle cells, formation of foam cells and platelets aggregation. This review highlights the causal role of neuropeptide Y and its receptor system in the development of diabetes mellitus and one of its complications: atherosclerotic cardiovascular disease. The information from this review provides both critical insights onto the mechanisms underlying the pathogenesis of atherosclerosis and evidence for the development of therapeutic strategies.

Type Journal
ISBN 1752-8984 (Electronic) 1479-1641 (Linking)
Authors Sun, W. W.; Zhu, P.; Shi, Y. C.; Zhang, C. L.; Huang, X. F.; Liang, S. Y.; Song, Z. Y.; Lin, S.
Responsible Garvan Author Associate Professor Yanchuan Shi
Publisher Name Diabetes & Vascular Disease Research
Published Date 2017-07-31
Published Volume 14
Published Issue 4
Published Pages 277-284
Status Published in-print
DOI 10.1177/1479164117704380
URL link to publisher's version https://www.ncbi.nlm.nih.gov/pubmed/28423914