The role of bilirubin and its protective function against coronary heart disease

Erkan, Aycan Fahri; Ekici, Berkay; Uğurlu, Murat; İş, Gürkan; Seker, Rabia; Demırtaş, Selda; Korkmaz, Şule

doi:10.1007/s00059-013-3872-5

Cited by 13 publications

(11 citation statements)

References 16 publications

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“…Unconjugated bilirubin (also known as indirect bilirubin, IBIL) is formed based on biliverdin reduction by biliverdin reductase (BVR) during heme catabolism where heme oxygenase (HO) catalyzes the initial and rate-limiting step (36,37). IBIL is then transported to the liver and conjugated with glucuronic acid by uridine diphosphate glucuronosyltransferase Family 1 Member A1 (UGT1A1) to a water-soluble form (DBIL) for elimination (38).…”

Section: Discussionmentioning

confidence: 99%

Serum Bilirubin Level as a Potential Marker for the Hearing Outcome in Severe-Profound Bilateral Sudden Deafness

Dai

Wang²,

Lan³

et al. 2019

Otology &Amp; Neurotology

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Section: Discussionmentioning

confidence: 99%

Serum Bilirubin Level as a Potential Marker for the Hearing Outcome in Severe-Profound Bilateral Sudden Deafness

Dai

Wang²,

Lan³

et al. 2019

Otology &Amp; Neurotology

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“…Both the antioxidant bilirubin and the vasodilator CO may contribute to this atheroprotective effect (Siow et al, 1999; Mayer, 2000; Parfenova et al, 2012; Erkan et al, 2013). Low bilirubin levels are associated with endothelial dysfunction and increased intima-media thickness (Erdogan et al, 2006), whereas high plasma bilirubin concentrations are linked to low incidence of cardiovascular disease (Schwertner et al, 1994) and stroke (Kimm et al, 2009).…”

Section: Altered Iron Homeostasis and Atherosclerosis: Epidemiologicamentioning

confidence: 99%

Atherogenesis and iron: from epidemiology to cellular level

et al. 2014

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Iron accumulates in human atherosclerotic lesions but whether it is a cause or simply a downstream consequence of the atheroma formation has been an open question for decades. According to the so called “iron hypothesis,” iron is believed to be detrimental for the cardiovascular system, thus promoting atherosclerosis development and progression. Iron, in its catalytically active form, can participate in the generation of reactive oxygen species and induce lipid-peroxidation, triggering endothelial activation, smooth muscle cell proliferation and macrophage activation; all of these processes are considered to be proatherogenic. On the other hand, the observation that hemochromatotic patients, affected by life-long iron overload, do not show any increased incidence of atherosclerosis is perceived as the most convincing evidence against the “iron hypothesis.” Epidemiological studies and data from animal models provided conflicting evidences about the role of iron in atherogenesis. Therefore, more careful studies are needed in which issues like the source and the compartmentalization of iron will be addressed. This review article summarizes what we have learnt about iron and atherosclerosis from epidemiological studies, animal models and cellular systems and highlights the rather contributory than innocent role of iron in atherogenesis.

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“…Bilirubin is generated by the action of the enzyme biliverdin reductase on biliverdin in the catabolism of heme [6], which contains indirect bilirubin (Ibil) and direct bilirubin (Dbil). Ibil is a bile pigment produced during the degredation of hemoproteins.…”

Section: Introductionmentioning

confidence: 99%

Protective and Indicating Effect of Indirect Bilirubin in Intracranial or Extracranial Artery Atherosclerotic Stenosis Progresses

Chen¹,

Zhang²,

Zhang³

et al. 2015

IJCM

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Background: Bilirubin is the metabolic end-product of heme degradation by heme oxygenase (HO), which has recently been shown to act as an antioxidant which can protect against atherosclerosis. This study explored the relationship between serum bilirubin levels and different degrees of atherosclerotic stenosis in intracranial or extracranial arteries. Methods: The study included 189 patients undergoing digital subtraction angiography (DSA) diagnosed as being normal or having been confirmed as atherosc lerotic stenosis in the intracranial or extracranial arteries. The patients were allocated to normal, mild (<50% diameter stenosis), moderate (50%-69% stenosis), severe (70%-99% stenosis) and occlusion groups according to the severity of stenosis proved by DSA. Blood samples were collected to determine bilirubin concentrations and other biochemical indicators of atherosclerosis. Univariate and multivariate analyses were performed to evaluate the associations between disease severity and biomarkers. Results: Indirect bilirubin (Ibil) concentrations increased in parallel with the increasing severity of atherosclerotic stenosis in the intracranial or extracranial arteries, but decreased in patients with occluded cranial vessels. Multivariate analysis showed that Ibil levels were significantly higher in patients with severe stenosis group than in those with mild stenosis (OR, 1.464; 95% CI, 1.050-2.042; P = 0.024). However, Ibil levels were significantly lower in patients with occlusion than in those with severe stenosis (OR, 0.790; 95% CI, 0.684-0.913; P = 0.001). Conclusions: Ibil appears to have a protective effect against the development of atherosclerotic stenosis in intracranial or extracranial arteries. The biosynthesis of Ibil increases with stenosis progresses but decreases once occlusion occurs.

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The role of bilirubin and its protective function against coronary heart disease

Cited by 13 publications

References 16 publications

Serum Bilirubin Level as a Potential Marker for the Hearing Outcome in Severe-Profound Bilateral Sudden Deafness

Serum Bilirubin Level as a Potential Marker for the Hearing Outcome in Severe-Profound Bilateral Sudden Deafness

Atherogenesis and iron: from epidemiology to cellular level

Protective and Indicating Effect of Indirect Bilirubin in Intracranial or Extracranial Artery Atherosclerotic Stenosis Progresses

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