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      Bilirubin in coronary artery disease: Cytotoxic or protective?

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          Abstract

          Bilirubin has traditionally been considered a cytotoxic waste product. However, recent studies have shown bilirubin to have anti-oxidant, anti-inflammatory, vasodilatory, anti-apoptotic and anti-proliferative functions. These properties potentially confer bilirubin a new role of protection especially in coronary artery disease (CAD), which is a low grade inflammatory process exacerbated by oxidative stress. In fact, recent literature reports an inverse relationship between serum concentration of bilirubin and the presence of CAD. In this article, we review the current literature exploring the association between levels of bilirubin and risk of CAD. We conclude that current evidence is inconclusive regarding the protective effect of bilirubin on CAD. A causal relationship between low serum bilirubin level and increased risk of CAD is not currently established.

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          Heme oxygenase-1: unleashing the protective properties of heme.

          Leo E. Otterbein, Miguel Soares, Kenichiro Yamashita … (2003)
          Heme oxygenase (HO)-1 catabolizes heme into three products: carbon monoxide (CO), biliverdin (which is rapidly converted to bilirubin) and free iron (which leads to the induction of ferritin, an iron-binding protein). HO-1 serves as a "protective" gene by virtue of the anti-inflammatory, anti-apoptotic and anti-proliferative actions of one or more of these three products. Administration of CO, biliverdin, bilirubin or iron-binding compounds is protective in rodent disease models of ischemia-reperfusion injury, allograft and xenograft survival, intimal hyperplasia following balloon injury or as seen in chronic graft rejection and others. We suggest that the products of HO-1 action could be valuable therapeutic agents and speculate that HO-1 functions as a "therapeutic funnel", mediating the beneficial effects attributed to other molecules, such as interleukin-10 (IL-10), inducible nitric oxide synthase (NOS2; iNOS) and prostaglandins. This Review is the third in a series on the regulation of the immune system by metabolic pathways.
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            Biliverdin reductase: a major physiologic cytoprotectant.

            David Barañano, Mahil Rao, Christopher Ferris … (2002)
            Bilirubin, an abundant pigment that causes jaundice, has long lacked any clear physiologic role. It arises from enzymatic reduction by biliverdin reductase of biliverdin, a product of heme oxygenase activity. Bilirubin is a potent antioxidant that we show can protect cells from a 10,000-fold excess of H2O2. We report that bilirubin is a major physiologic antioxidant cytoprotectant. Thus, cellular depletion of bilirubin by RNA interference markedly augments tissue levels of reactive oxygen species and causes apoptotic cell death. Depletion of glutathione, generally regarded as a physiologic antioxidant cytoprotectant, elicits lesser increases in reactive oxygen species and cell death. The potent physiologic antioxidant actions of bilirubin reflect an amplification cycle whereby bilirubin, acting as an antioxidant, is itself oxidized to biliverdin and then recycled by biliverdin reductase back to bilirubin. This redox cycle may constitute the principal physiologic function of bilirubin.
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              The enzymatic conversion of heme to bilirubin by microsomal heme oxygenase.

              R Tenhunen, H Marver, R SCHMID (1968)
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                Author and article information

                Journal
                Journal ID (nlm-ta): World J Gastrointest Pharmacol Ther
                Journal ID (publisher-id): WJGPT
                Title: World Journal of Gastrointestinal Pharmacology and Therapeutics
                Publisher: Baishideng Publishing Group Inc
                ISSN (Electronic): 2150-5349
                Publication date (Print): 6 November 2016
                Publication date (Electronic): 6 November 2016
                Volume: 7
                Issue: 4
                Pages: 469-476
                Affiliations
                Nancy Gupta, Sachin Sule, Department of Medicine, Westchester Medical Center, New York Medical College, Valhalla, NY 10595, United States
                Tavankit Singh, Department of Medicine, Cleveland Clinic, Cleveland, OH 44195, United States
                Rahul Chaudhary, Department of Medicine, Sinai Hospital of Baltimore, Johns Hopkins University, Baltimore, MD 21218, United States
                Sushil K Garg, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, United States
                Gurprataap Singh Sandhu, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15260, United States
                Varun Mittal, Einstein Healthcare Network, Philadelphia, PA 19141, United States
                Rahul Gupta, Government Medical College, Amritsar, Punjab 143001, India
                Roxana Bodin, Division of Gastroenterology and Hepatobiliary Disease, New York Medical College, Valhalla, NY 10595, United States
                Author notes

                Author contributions: All authors contributed to the manuscript; Gupta N, Singh T and Chaudhary R have contributed equally for the paper.

                Correspondence to: Nancy Gupta, MD, Department of Medicine, Westchester Medical Center, New York Medical College, 40 Sunshine Cottage Rd, Valhalla, NY 10595, United States. drnancygupta87@ 123456gmail.com

                Telephone: +1-914-5361563 Fax: +1-914-4935827

                Article
                Other ID: jWJGPT.v7.i4.pg469
                DOI: 10.4292/wjgpt.v7.i4.469
                PMC ID: 5095566
                SO-VID: 48141286-af0c-4a2a-afc8-9bb94b8c1e2f
                Copyright © ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
                License:

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                Date received : 2 April 2016
                Date revision received : 7 June 2016
                Date accepted : 27 August 2016
                Categories
                Subject: Review

                Keywords: bilirubin,cytotoxic,protective,anti-oxidant,anti-inflammatory,anti coronary artery disease,lipid peroxidation,gilbert
                Data availability:
                Keywords: bilirubin, cytotoxic, protective, anti-oxidant, anti-inflammatory, anti coronary artery disease, lipid peroxidation, gilbert

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