Bile acids and cardiovascular function in cirrhosis

被引:46
作者
Voiosu, Andrei [1 ,2 ,3 ]
Wiese, Signe [1 ,4 ]
Voiosu, Theodor [2 ,3 ]
Bendtsen, Flemming [4 ,5 ]
Moller, Soren [1 ,4 ]
机构
[1] Hvidovre Univ Hosp, Dept Clin Physiol & Nucl Med, Ctr Funct & Diagnost Imaging & Res, Hvidovre, Denmark
[2] Colentina Clin Hosp, Dept Gastroenterol & Hepatol, Bucharest, Romania
[3] Carol Davila Univ Med & Pharm, Bucharest, Romania
[4] Univ Copenhagen, Fac Hlth Sci, Copenhagen, Denmark
[5] Hvidovre Univ Hosp, Div Med, Gastro Unit, Hvidovre, Denmark
关键词
bile acids; cholestasis; cirrhosis; cirrhotic cardiomyopathy; farnesoid X-activated receptor; hemodynamics; ursodeoxycholic acid; FARNESOID-X-RECEPTOR; PRIMARY BILIARY-CIRRHOSIS; VASCULAR SMOOTH-MUSCLE; PROTEIN-COUPLED RECEPTOR; AGONIST OBETICHOLIC ACID; PLACEBO-CONTROLLED TRIAL; FXR-MEDIATED REGULATION; URSODEOXYCHOLIC ACID; LIVER-CIRRHOSIS; IN-VITRO;
D O I
10.1111/liv.13394
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Cirrhotic cardiomyopathy and the hyperdynamic syndrome are clinically important complications of cirrhosis, but their exact pathogenesis is still partly unknown. Experimental models have proven the cardiotoxic effects of bile acids and recent studies of their varied receptor-mediated functions offer new insight into their involvement in cardiovascular dysfunction in cirrhosis. Bile acid receptors such as farnesoid X-activated receptor and TGR5 are currently under investigation as potential therapeutic targets in a variety of pathological conditions. These receptors have also recently been identified in cardiomyocytes, vascular endothelial cells and smooth muscle cells where they seem to play an important role in cellular metabolism. Chronic cholestasis leading to abnormal levels of circulating bile acids alters the normal signalling pathways and contributes to the development of profound cardiovascular disturbances. This review summarizes the evidence regarding the role of bile acids and their receptors in the generation of cardiovascular dysfunction in cirrhosis.
引用
收藏
页码:1420 / 1430
页数:11
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