Bilirubin acts as a multipotent guardian of cardiovascular integrity: more than just a radical idea

被引:50
|
作者
Bulmer, Andrew C. [1 ,2 ]
Bakrania, Bhavisha [3 ]
Du Toit, Eugene F. [1 ,2 ]
Boon, Ai-Ching [1 ,2 ]
Clark, Paul J. [4 ,5 ]
Powell, Lawrie W. [6 ]
Wagner, Karl-Heinz [7 ]
Headrick, John P. [1 ,2 ]
机构
[1] Griffith Univ, Sch Med Sci, Gold Coast Campus, Gold Coast, Qld 4222, Australia
[2] Griffith Univ, Menzies Hlth Inst Queensland, Gold Coast Campus, Gold Coast, Qld 4222, Australia
[3] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA
[4] Univ Queensland, Sch Med, QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia
[5] Princess Alexandra & Mater Hosp, Brisbane, Qld, Australia
[6] Univ Queensland, Royal Brisbane & Womens Hosp, Ctr Adv Clin Res, Ctr Clin Res, Brisbane, Qld, Australia
[7] Univ Vienna, Dept Nutr Sci, Vienna, Austria
关键词
atherosclerosis; heart; heme oxygenase; hepatic; lipid; PERCUTANEOUS CORONARY INTERVENTION; GABA/GLYCINERGIC SYNAPTIC-TRANSMISSION; ELEVATION MYOCARDIAL-INFARCTION; VENTRAL COCHLEAR NUCLEUS; GILBERTS-SYNDROME; SERUM BILIRUBIN; UNCONJUGATED BILIRUBIN; PLATELET ACTIVATION; NITRIC-OXIDE; GUNN RAT;
D O I
10.1152/ajpheart.00417.2017
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Bilirubin, a potentially toxic catabolite of heme and indicator of hepatobiliary insufficiency, exhibits potent cardiac and vascular protective properties. Individuals with Gilbert's syndrome (GS) may experience hyperbilirubinemia in response to stressors including reduced hepatic bilirubin excretion/increased red blood cell breakdown, with individuals usually informed by their clinician that their condition is of little consequence. However, GS appears to protect from all-cause mortality, with progressively elevated total bilirubin associated with protection from ischemic heart and chronic obstructive pulmonary diseases. Bilirubin may protect against these diseases and associated mortality by reducing circulating cholesterol, oxidative lipid/protein modifications, and blood pressure. In addition, bilirubin inhibits platelet activation and protects the heart from ischemia-reperfusion injury. These effects attenuate multiple stages of the atherosclerotic process in addition to protecting the heart during resultant ischemic stress, likely underpinning the profound reduction in cardiovascular mortality in hyperbilirubinemic GS. This review outlines our current knowledge of and uses for bilirubin in clinical medicine and summarizes recent progress in revealing the physiological importance of this poorly understood molecule. We believe that this review will be of significant interest to clinicians, medical researchers, and individuals who have GS.
引用
收藏
页码:H429 / H447
页数:19
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