Endotheliopathy in the metabolic syndrome: Mechanisms and clinical implications

被引:12
|
作者
Furuta, Kunimaro [1 ,2 ]
Tang, Xiaofang [3 ]
Islam, Shahidul [1 ]
Tapia, Alonso [3 ]
Chen, Zhen Bouman [3 ,6 ]
Ibrahim, Samar H. [1 ,4 ,5 ]
机构
[1] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA
[2] Osaka Univ Grad Sch Med, Dept Gastroenterol & Hepatol, Osaka, Japan
[3] City Hope Comprehens Canc Ctr, Dept Diabet Complicat & Metab, Duarte, CA USA
[4] Mayo Clin, Div Pediat Gastroenterol & Hepatol, Rochester, MN USA
[5] Mayo Clin, Dept Pediat & Adolescent Med, Div Pediat Gastroenterol, 200 First St SW, Rochester, MN 55905 USA
[6] City Hope Natl Med Ctr, Arther Riggs Diabet Metab Res Inst, Dept Diabet Complicat & Metab, 1500 E Duarte Rd, Duarte, CA 91010 USA
基金
美国国家卫生研究院;
关键词
Metabolic syndrome (MetS); Endotheliopathy; Endothelial cell (EC); Liver sinusoidal endothelial cell (LSEC); Adipose tissue (AT); Nonalcoholic fatty liver disease (NAFLD); Nonalcoholic steatohepatitis (NASH); Capillarization; Inflammation; Fibrosis; Endothelial-to-mesenchymal transition; (EndoMT); MESENCHYMAL TRANSITION CONTRIBUTES; FATTY LIVER-DISEASE; GROWTH-FACTOR; NONALCOHOLIC STEATOHEPATITIS; INSULIN-RESISTANCE; HEPATIC-FIBROSIS; CELL ACTIVATION; VEGF-A; DYSFUNCTION; OBESITY;
D O I
10.1016/j.pharmthera.2023.108372
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The increasing prevalence of the metabolic syndrome (MetS) is a threat to global public health due to its lethal complications. Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the MetS characterized by hepatic steatosis, which is potentially progressive to the inflammatory and fibrotic nonalcoholic steatohepa-titis (NASH). The adipose tissue (AT) is also a major metabolic organ responsible for the regulation of whole -body energy homeostasis, and thereby highly involved in the pathogenesis of the MetS. Recent studies suggest that endothelial cells (ECs) in the liver and AT are not just inert conduits but also crucial mediators in various bi-ological processes via the interaction with other cell types in the microenvironment both under physiological and pathological conditions. Herein, we highlight the current knowledge of the role of the specialized liver sinusoidal endothelial cells (LSECs) in NAFLD pathophysiology. Next, we discuss the processes through which AT EC dys-function leads to MetS progression, with a focus on inflammation and angiogenesis in the AT as well as on endothelial-to-mesenchymal transition of AT-ECs. In addition, we touch upon the function of ECs residing in other metabolic organs including the pancreatic islet and the gut, the dysregulation of which may also contribute to the MetS. Finally, we highlight potential EC-based therapeutic targets for human MetS, and NASH based on recent achievements in basic and clinical research and discuss how to approach unsolved problems in the field.(c) 2023 Elsevier Inc. All rights reserved.
引用
收藏
页数:12
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