Overview of bile acid signaling in the cardiovascular system
- PMID: 33521099
- PMCID: PMC7812903
- DOI: 10.12998/wjcc.v9.i2.308
Overview of bile acid signaling in the cardiovascular system
Abstract
Bile acids (BAs) are classically known to play a vital role in the metabolism of lipids and in absorption. It is now well established that BAs act as signaling molecules, activating different receptors (such as farnesoid X receptor, vitamin D receptor, Takeda G-protein-coupled receptor 5, sphingosine-1-phosphate, muscarinic receptors, and big potassium channels) and participating in the regulation of energy homeostasis and lipid and glucose metabolism. In addition, increased BAs can impair cardiovascular function in liver cirrhosis. Approximately 50% of patients with cirrhosis develop cirrhotic cardiomyopathy. Exposure to high concentrations of hydrophobic BAs has been shown to be related to adverse effects with respect to vascular tension, endothelial function, arrhythmias, coronary atherosclerotic heart disease, and heart failure. The BAs in the serum BA pool have relevant through their hydrophobicity, and the lipophilic BAs are more harmful to the heart. Interestingly, ursodeoxycholic acid is a hydrophilic BA, and it is used as a therapeutic drug to reverse and protect the harmful cardiac effects caused by hydrophobic elevated BAs. In order to elucidate the mechanism of BAs and cardiovascular function, abundant experiments have been conducted in vitro and in vivo. The aim of this review was to explore the mechanism of BAs in the cardiovascular system.
Keywords: Arteries; Bile acids; Cardiovascular; Cirrhosis; Receptors; Signaling.
©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
Conflict of interest statement
Conflict-of-interest statement: All authors declare that: (1) No support, financial or otherwise, has been received from any organization that may have an interest in the submitted work; and (2) There are no other relationships or activities that could appear to have influenced the submitted work.
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