胆红素
医学
氧化应激
内科学
心脏病学
内分泌学
免疫学
作者
Andrew C. Bulmer,Bhavisha Bakrania,Eugene F. du Toit,Ai‐Ching Boon,Paul J. Clark,Lawrie W. Powell,Karl‐Heinz Wagner,John P. Headrick
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology
[American Physical Society]
日期:2018-03-30
卷期号:315 (3): H429-H447
被引量:59
标识
DOI:10.1152/ajpheart.00417.2017
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.
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