Effect of asymmetric dimethylarginine (ADMA) on heart failure development
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability and can increase production of NOS derived reactive oxidative species. Increased plasma ADMA is a one of the strongest predictors of mortality in patients who have had a m...
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| Veröffentlicht in: | Nitric oxide 2016-04, Vol.54, p.73-81 |
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| creator | Liu, Xiaoyu Hou, Lei Xu, Dachun Chen, Angela Yang, Liuqing Zhuang, Yan Xu, Yawei Fassett, John T. Chen, Yingjie |
| description | Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability and can increase production of NOS derived reactive oxidative species. Increased plasma ADMA is a one of the strongest predictors of mortality in patients who have had a myocardial infarction or suffer from chronic left heart failure, and is also an independent risk factor for several other conditions that contribute to heart failure development, including hypertension, coronary artery disease/atherosclerosis, diabetes, and renal dysfunction. The enzyme responsible for ADMA degradation is dimethylarginine dimethylaminohydrolase-1 (DDAH1). DDAH1 plays an important role in maintaining nitric oxide bioavailability and preserving cardiovascular function in the failing heart. Here, we examine mechanisms of abnormal NO production in heart failure, with particular focus on the role of ADMA and DDAH1.
•ADMA may exacerbate heart failure development directly.•ADMA may exacerbate heart failure through increase of cardiovascular risk factors.•DDAH1 plays a critical role in ADMA degradation. |
| doi_str_mv | 10.1016/j.niox.2016.02.006 |
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•ADMA may exacerbate heart failure development directly.•ADMA may exacerbate heart failure through increase of cardiovascular risk factors.•DDAH1 plays a critical role in ADMA degradation.</description><identifier>ISSN: 1089-8603</identifier><identifier>EISSN: 1089-8611</identifier><identifier>DOI: 10.1016/j.niox.2016.02.006</identifier><identifier>PMID: 26923818</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amidohydrolases - genetics ; Amidohydrolases - metabolism ; Animals ; Arginine - analogs & derivatives ; Arginine - metabolism ; Asymmetric dimethylarginine ; Dimethylarginine dimethylaminohydrolase-1 ; Heart failure ; Heart Failure - etiology ; Heart Failure - metabolism ; Humans ; Nitric oxide ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - antagonists & inhibitors ; omega-N-Methylarginine - metabolism ; Peroxynitrous Acid - metabolism ; Signal Transduction ; Superoxides - metabolism</subject><ispartof>Nitric oxide, 2016-04, Vol.54, p.73-81</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-45cf63f4b903a932bf4918a85d6d764bb3a3a4dd96bfabd7a455342f65b2d2cf3</citedby><cites>FETCH-LOGICAL-c521t-45cf63f4b903a932bf4918a85d6d764bb3a3a4dd96bfabd7a455342f65b2d2cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S108986031630012X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26923818$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xiaoyu</creatorcontrib><creatorcontrib>Hou, Lei</creatorcontrib><creatorcontrib>Xu, Dachun</creatorcontrib><creatorcontrib>Chen, Angela</creatorcontrib><creatorcontrib>Yang, Liuqing</creatorcontrib><creatorcontrib>Zhuang, Yan</creatorcontrib><creatorcontrib>Xu, Yawei</creatorcontrib><creatorcontrib>Fassett, John T.</creatorcontrib><creatorcontrib>Chen, Yingjie</creatorcontrib><title>Effect of asymmetric dimethylarginine (ADMA) on heart failure development</title><title>Nitric oxide</title><addtitle>Nitric Oxide</addtitle><description>Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability and can increase production of NOS derived reactive oxidative species. Increased plasma ADMA is a one of the strongest predictors of mortality in patients who have had a myocardial infarction or suffer from chronic left heart failure, and is also an independent risk factor for several other conditions that contribute to heart failure development, including hypertension, coronary artery disease/atherosclerosis, diabetes, and renal dysfunction. The enzyme responsible for ADMA degradation is dimethylarginine dimethylaminohydrolase-1 (DDAH1). DDAH1 plays an important role in maintaining nitric oxide bioavailability and preserving cardiovascular function in the failing heart. Here, we examine mechanisms of abnormal NO production in heart failure, with particular focus on the role of ADMA and DDAH1.
•ADMA may exacerbate heart failure development directly.•ADMA may exacerbate heart failure through increase of cardiovascular risk factors.•DDAH1 plays a critical role in ADMA degradation.</description><subject>Amidohydrolases - genetics</subject><subject>Amidohydrolases - metabolism</subject><subject>Animals</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - metabolism</subject><subject>Asymmetric dimethylarginine</subject><subject>Dimethylarginine dimethylaminohydrolase-1</subject><subject>Heart failure</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - metabolism</subject><subject>Humans</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>omega-N-Methylarginine - metabolism</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Signal Transduction</subject><subject>Superoxides - metabolism</subject><issn>1089-8603</issn><issn>1089-8611</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLw0AUhQdRbH38ARcyS10kziOZJCBCqVULFTe6HubZTkkyZZIW---dUi26cXUP3HPO5X4AXGGUYoTZ3TJtnf9MSdQpIilC7AgMMSqrpGQYHx80ogNw1nVLhFBGS3YKBoRVhJa4HILpxFqjeugtFN22aUwfnILaRbHY1iLMXetaA29Gj6-jW-hbuDAi9NAKV6-DgdpsTO1XjWn7C3BiRd2Zy-95Dj6eJu_jl2T29jwdj2aJygnukyxXllGbyQpRUVEibVbhUpS5ZrpgmZRUUJFpXTFphdSFyPKcZsSyXBJNlKXn4GHfu1rLxmgVTwdR81VwjQhb7oXjfzetW_C53_Ac4aKoaCwg-wIVfNcFYw9ZjPgOLF_yHVi-A8sR4RFsDF3_vnqI_JCMhvu9wcTfN84E3ilnWmW0CxEw19791_8Fv-GMAg</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Liu, Xiaoyu</creator><creator>Hou, Lei</creator><creator>Xu, Dachun</creator><creator>Chen, Angela</creator><creator>Yang, Liuqing</creator><creator>Zhuang, Yan</creator><creator>Xu, Yawei</creator><creator>Fassett, John T.</creator><creator>Chen, Yingjie</creator><general>Elsevier Inc</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>5PM</scope></search><sort><creationdate>20160401</creationdate><title>Effect of asymmetric dimethylarginine (ADMA) on heart failure development</title><author>Liu, Xiaoyu ; Hou, Lei ; Xu, Dachun ; Chen, Angela ; Yang, Liuqing ; Zhuang, Yan ; Xu, Yawei ; Fassett, John T. ; Chen, Yingjie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-45cf63f4b903a932bf4918a85d6d764bb3a3a4dd96bfabd7a455342f65b2d2cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Amidohydrolases - genetics</topic><topic>Amidohydrolases - metabolism</topic><topic>Animals</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - metabolism</topic><topic>Asymmetric dimethylarginine</topic><topic>Dimethylarginine dimethylaminohydrolase-1</topic><topic>Heart failure</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - metabolism</topic><topic>Humans</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>omega-N-Methylarginine - metabolism</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Signal Transduction</topic><topic>Superoxides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xiaoyu</creatorcontrib><creatorcontrib>Hou, Lei</creatorcontrib><creatorcontrib>Xu, Dachun</creatorcontrib><creatorcontrib>Chen, Angela</creatorcontrib><creatorcontrib>Yang, Liuqing</creatorcontrib><creatorcontrib>Zhuang, Yan</creatorcontrib><creatorcontrib>Xu, Yawei</creatorcontrib><creatorcontrib>Fassett, John T.</creatorcontrib><creatorcontrib>Chen, Yingjie</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nitric oxide</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xiaoyu</au><au>Hou, Lei</au><au>Xu, Dachun</au><au>Chen, Angela</au><au>Yang, Liuqing</au><au>Zhuang, Yan</au><au>Xu, Yawei</au><au>Fassett, John T.</au><au>Chen, Yingjie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of asymmetric dimethylarginine (ADMA) on heart failure development</atitle><jtitle>Nitric oxide</jtitle><addtitle>Nitric Oxide</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>54</volume><spage>73</spage><epage>81</epage><pages>73-81</pages><issn>1089-8603</issn><eissn>1089-8611</eissn><abstract>Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability and can increase production of NOS derived reactive oxidative species. Increased plasma ADMA is a one of the strongest predictors of mortality in patients who have had a myocardial infarction or suffer from chronic left heart failure, and is also an independent risk factor for several other conditions that contribute to heart failure development, including hypertension, coronary artery disease/atherosclerosis, diabetes, and renal dysfunction. The enzyme responsible for ADMA degradation is dimethylarginine dimethylaminohydrolase-1 (DDAH1). DDAH1 plays an important role in maintaining nitric oxide bioavailability and preserving cardiovascular function in the failing heart. Here, we examine mechanisms of abnormal NO production in heart failure, with particular focus on the role of ADMA and DDAH1.
•ADMA may exacerbate heart failure development directly.•ADMA may exacerbate heart failure through increase of cardiovascular risk factors.•DDAH1 plays a critical role in ADMA degradation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26923818</pmid><doi>10.1016/j.niox.2016.02.006</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amidohydrolases - genetics Amidohydrolases - metabolism Animals Arginine - analogs & derivatives Arginine - metabolism Asymmetric dimethylarginine Dimethylarginine dimethylaminohydrolase-1 Heart failure Heart Failure - etiology Heart Failure - metabolism Humans Nitric oxide Nitric Oxide - biosynthesis Nitric Oxide Synthase - antagonists & inhibitors omega-N-Methylarginine - metabolism Peroxynitrous Acid - metabolism Signal Transduction Superoxides - metabolism |
| title | Effect of asymmetric dimethylarginine (ADMA) on heart failure development |
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