Bilirubin and Endothelial Function
Bilirubin is a fundamental metabolic end product of heme degradation. Despite acting as a cytotoxic metabolite at high concentrations, bilirubin at physiological concentrations has antioxidant effects, such as scavenging reactive oxygen species, leading to a decrease in oxidative stress. Endothelial...
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| Veröffentlicht in: | Journal of Atherosclerosis and Thrombosis 2019/08/01, Vol.26(8), pp.688-696 |
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| container_end_page | 696 |
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| container_issue | 8 |
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| container_title | Journal of Atherosclerosis and Thrombosis |
| container_volume | 26 |
| creator | Maruhashi, Tatsuya Kihara, Yasuki Higashi, Yukihito |
| description | Bilirubin is a fundamental metabolic end product of heme degradation. Despite acting as a cytotoxic metabolite at high concentrations, bilirubin at physiological concentrations has antioxidant effects, such as scavenging reactive oxygen species, leading to a decrease in oxidative stress. Endothelial dysfunction is an early feature of and plays an important role in the development and progression of atherosclerosis, leading to cardiovascular complications. One mechanism of endothelial dysfunction is an increase in oxidative stress, by which the bioavailability of nitric oxide is decreased. Therefore, bilirubin is expected to improve endothelial function, to inhibit the progression of atherosclerosis, and to reduce cardiovascular complications by inactivating oxidative stress through its antioxidant effects. In this review, we will focus on the clinical associations of the antioxidant bilirubin with endothelial function and cardiovascular complications. |
| doi_str_mv | 10.5551/jat.RV17035 |
| format | Article |
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Despite acting as a cytotoxic metabolite at high concentrations, bilirubin at physiological concentrations has antioxidant effects, such as scavenging reactive oxygen species, leading to a decrease in oxidative stress. Endothelial dysfunction is an early feature of and plays an important role in the development and progression of atherosclerosis, leading to cardiovascular complications. One mechanism of endothelial dysfunction is an increase in oxidative stress, by which the bioavailability of nitric oxide is decreased. Therefore, bilirubin is expected to improve endothelial function, to inhibit the progression of atherosclerosis, and to reduce cardiovascular complications by inactivating oxidative stress through its antioxidant effects. In this review, we will focus on the clinical associations of the antioxidant bilirubin with endothelial function and cardiovascular complications.</description><identifier>ISSN: 1340-3478</identifier><identifier>EISSN: 1880-3873</identifier><identifier>DOI: 10.5551/jat.RV17035</identifier><identifier>PMID: 31270300</identifier><language>eng</language><publisher>Japan: Japan Atherosclerosis Society</publisher><subject>Animals ; Antioxidant ; Antioxidants - metabolism ; Bilirubin ; Bilirubin - metabolism ; Endothelial function ; Endothelium, Vascular - cytology ; Endothelium, Vascular - physiology ; Gilbert's syndrome ; Humans ; Oxidative stress ; Review ; Vascular Diseases - physiopathology</subject><ispartof>Journal of Atherosclerosis and Thrombosis, 2019/08/01, Vol.26(8), pp.688-696</ispartof><rights>2019 This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.</rights><rights>2019 Japan Atherosclerosis Society 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c694t-98d27bba992129547ebcb09cee8d88969ceb85c1fb13dfe78dff6738ff79fb4b3</citedby><cites>FETCH-LOGICAL-c694t-98d27bba992129547ebcb09cee8d88969ceb85c1fb13dfe78dff6738ff79fb4b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6711845/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6711845/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,1883,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31270300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maruhashi, Tatsuya</creatorcontrib><creatorcontrib>Kihara, Yasuki</creatorcontrib><creatorcontrib>Higashi, Yukihito</creatorcontrib><creatorcontrib>Department of Cardiovascular Medicine</creatorcontrib><creatorcontrib>Research Institute for Radiation Biology and Medicine</creatorcontrib><creatorcontrib>Department of Cardiovascular Regeneration and Medicine</creatorcontrib><creatorcontrib>Division of Regeneration and Medicine</creatorcontrib><creatorcontrib>Graduate School of Biomedical and Health Sciences</creatorcontrib><creatorcontrib>Hiroshima University</creatorcontrib><creatorcontrib>Hiroshima University Hospital</creatorcontrib><title>Bilirubin and Endothelial Function</title><title>Journal of Atherosclerosis and Thrombosis</title><addtitle>JAT</addtitle><description>Bilirubin is a fundamental metabolic end product of heme degradation. Despite acting as a cytotoxic metabolite at high concentrations, bilirubin at physiological concentrations has antioxidant effects, such as scavenging reactive oxygen species, leading to a decrease in oxidative stress. Endothelial dysfunction is an early feature of and plays an important role in the development and progression of atherosclerosis, leading to cardiovascular complications. One mechanism of endothelial dysfunction is an increase in oxidative stress, by which the bioavailability of nitric oxide is decreased. Therefore, bilirubin is expected to improve endothelial function, to inhibit the progression of atherosclerosis, and to reduce cardiovascular complications by inactivating oxidative stress through its antioxidant effects. In this review, we will focus on the clinical associations of the antioxidant bilirubin with endothelial function and cardiovascular complications.</description><subject>Animals</subject><subject>Antioxidant</subject><subject>Antioxidants - metabolism</subject><subject>Bilirubin</subject><subject>Bilirubin - metabolism</subject><subject>Endothelial function</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - physiology</subject><subject>Gilbert's syndrome</subject><subject>Humans</subject><subject>Oxidative stress</subject><subject>Review</subject><subject>Vascular Diseases - physiopathology</subject><issn>1340-3478</issn><issn>1880-3873</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkdtrVDEQxoMotlaffJfFJ0G25nJyexFq6UUoCKK-hiRn0s2STWpyTrH_vdnuulQImQ_mxzfDNwi9JfiUc04-re10-v0XkZjxZ-iYKIWXTEn2vGs2dD1IdYRetbbGmDHO6Ut0xAjtOMbH6P2XmGKdXcwLm8fFRR7LtIIUbVpcztlPseTX6EWwqcGbfT1BPy8vfpxfL2--XX09P7tZeqGHaanVSKVzVmtKqOaDBOcd1h5AjUpp0ZVT3JPgCBsDSDWGICRTIUgd3ODYCfq8872b3QZGD3mqNpm7Gje2Pphio_m_k-PK3JZ7IyQhauDd4MPeoJbfM7TJbGLzkJLNUOZmKOX9Kf6IftyhvpbWKoTDGILNNlXTUzX7VDv97ulmB_ZfjB242gG9G71NJaeYwazLXHOPzMAfOZbNgzUUE20wpgKrbTFYqC6EFv0yjDHanc52Tus22Vs4jLJ1ij7B41pUGLX99usden5lq4HM_gLuHaGk</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Maruhashi, Tatsuya</creator><creator>Kihara, Yasuki</creator><creator>Higashi, Yukihito</creator><general>Japan Atherosclerosis Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190801</creationdate><title>Bilirubin and Endothelial Function</title><author>Maruhashi, Tatsuya ; Kihara, Yasuki ; Higashi, Yukihito</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c694t-98d27bba992129547ebcb09cee8d88969ceb85c1fb13dfe78dff6738ff79fb4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antioxidant</topic><topic>Antioxidants - metabolism</topic><topic>Bilirubin</topic><topic>Bilirubin - metabolism</topic><topic>Endothelial function</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - physiology</topic><topic>Gilbert's syndrome</topic><topic>Humans</topic><topic>Oxidative stress</topic><topic>Review</topic><topic>Vascular Diseases - physiopathology</topic><toplevel>online_resources</toplevel><creatorcontrib>Maruhashi, Tatsuya</creatorcontrib><creatorcontrib>Kihara, Yasuki</creatorcontrib><creatorcontrib>Higashi, Yukihito</creatorcontrib><creatorcontrib>Department of Cardiovascular Medicine</creatorcontrib><creatorcontrib>Research Institute for Radiation Biology and Medicine</creatorcontrib><creatorcontrib>Department of Cardiovascular Regeneration and Medicine</creatorcontrib><creatorcontrib>Division of Regeneration and Medicine</creatorcontrib><creatorcontrib>Graduate School of Biomedical and Health Sciences</creatorcontrib><creatorcontrib>Hiroshima University</creatorcontrib><creatorcontrib>Hiroshima University Hospital</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Atherosclerosis and Thrombosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maruhashi, Tatsuya</au><au>Kihara, Yasuki</au><au>Higashi, Yukihito</au><aucorp>Department of Cardiovascular Medicine</aucorp><aucorp>Research Institute for Radiation Biology and Medicine</aucorp><aucorp>Department of Cardiovascular Regeneration and Medicine</aucorp><aucorp>Division of Regeneration and Medicine</aucorp><aucorp>Graduate School of Biomedical and Health Sciences</aucorp><aucorp>Hiroshima University</aucorp><aucorp>Hiroshima University Hospital</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bilirubin and Endothelial Function</atitle><jtitle>Journal of Atherosclerosis and Thrombosis</jtitle><addtitle>JAT</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>26</volume><issue>8</issue><spage>688</spage><epage>696</epage><pages>688-696</pages><issn>1340-3478</issn><eissn>1880-3873</eissn><abstract>Bilirubin is a fundamental metabolic end product of heme degradation. Despite acting as a cytotoxic metabolite at high concentrations, bilirubin at physiological concentrations has antioxidant effects, such as scavenging reactive oxygen species, leading to a decrease in oxidative stress. Endothelial dysfunction is an early feature of and plays an important role in the development and progression of atherosclerosis, leading to cardiovascular complications. One mechanism of endothelial dysfunction is an increase in oxidative stress, by which the bioavailability of nitric oxide is decreased. Therefore, bilirubin is expected to improve endothelial function, to inhibit the progression of atherosclerosis, and to reduce cardiovascular complications by inactivating oxidative stress through its antioxidant effects. In this review, we will focus on the clinical associations of the antioxidant bilirubin with endothelial function and cardiovascular complications.</abstract><cop>Japan</cop><pub>Japan Atherosclerosis Society</pub><pmid>31270300</pmid><doi>10.5551/jat.RV17035</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1340-3478 1880-3873 |
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| subjects | Animals Antioxidant Antioxidants - metabolism Bilirubin Bilirubin - metabolism Endothelial function Endothelium, Vascular - cytology Endothelium, Vascular - physiology Gilbert's syndrome Humans Oxidative stress Review Vascular Diseases - physiopathology |
| title | Bilirubin and Endothelial Function |
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