Journal article
Endothelial dysfunction in atherosclerotic cardiovascular diseases and beyond: From mechanism to pharmacotherapies
S Xu, I Ilyas, PJ Little, H Li, D Kamato, X Zheng, S Luo, Z Li, P Liu, J Han, IC Harding, EE Ebong, SJ Cameron, AG Stewart, J Weng
Pharmacological Reviews | Published : 2021
Abstract
The endothelium, a cellular monolayer lining the blood vessel wall, plays a critical role in maintaining multiorgan health and homeostasis. Endothelial functions in health include dynamic maintenance of vascular tone, angiogenesis, hemostasis, and the provision of an antioxidant, anti-inflammatory, and antithrombotic interface. Dysfunction of the vascular endothelium presents with impaired endothelium-dependent vasodilation, heightened oxidative stress, chronic inflammation, leukocyte adhesion and hyper-permeability, and endothelial cell senescence. Recent studies have implicated altered endothelial cell metabolism and endothelial-to-mesenchymal transition as new features of endothelial dysf..
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Grants
Awarded by Guangdong Provincial Pearl River Talents Program
Funding Acknowledgements
This study was supported by National Natural Science Foundation of China [Grant 82070464] (to S.X.), [Grants 81941022 and 81530025] (to J.W.), and [Grant 81903606] (to H.L.); Strategic Priority Research Program of Chinese Academy of Sciences [Grant XDB38010100] (to J.W.); and the National Key R&D Program of China [Grant 2017YFC1309603] (to J.W.). This work was also supported by Program for Innovative Research Team of The First Affiliated Hospital of USTC [Grant CXGG02] (to J.W.), Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program [2017BT01S131], China International Medical Foundation (to X.Z.), Natural Science Foundation of Anhui Province [Grant 006223066002] (to S.L.), and Natural Science Foundation of Guangdong Province [Grant 2017A030310542] (to H.L.). This work was also supported by grants from the United States government's National Science Foundation [CMMI-1846962] (awarded to E.E.E.) and Australian Research Council [IC170100016] (to A.G.S.).