Adrenomedullin: regulator of systemic and cardiac homeostasis in acute myocardial infarction
During and following acute myocardial infarction, a variety of endogenous mediators are elevated, one of which is adrenomedullin (AM). AM is a multifunctional peptide that has been identified as having a putative beneficial role following an ischemic insult at both systemic and local levels. Classic...
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Veröffentlicht in: | Pharmacology & therapeutics (Oxford) 2005-02, Vol.105 (2), p.95-112 |
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description | During and following acute myocardial infarction, a variety of endogenous mediators are elevated, one of which is adrenomedullin (AM). AM is a multifunctional peptide that has been identified as having a putative beneficial role following an ischemic insult at both systemic and local levels. Classically described as a potent vasodilator, natriuretic, and diuretic agent, experimental infarct models also demonstrate AM to exhibit antiproliferative and antiapoptotic functions in the myocardium, counterregulating the effects of mediators such as angiotensin-II and endothelin-1. Less well documented are the angiogenic and inflammatory modulating potentials of AM, which may also contribute toward reducing adverse ventricular remodeling. The review examines clinical and experimental studies, looking at the effects of AM and cellular mechanisms that could be involved in mediating cardioprotective effects and ultimately optimizing left ventricular remodeling. Finally, the possibility of enhancing endogenous actions of AM by pharmacological intervention is considered. |
doi_str_mv | 10.1016/j.pharmthera.2004.08.012 |
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Finally, the possibility of enhancing endogenous actions of AM by pharmacological intervention is considered.</description><subject>Adrenomedullin</subject><subject>Animals</subject><subject>Cell Survival</subject><subject>Coronary Vessels - metabolism</subject><subject>Coronary Vessels - physiopathology</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Inflammation Mediators - metabolism</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Oxidative Stress</subject><subject>Peptides - physiology</subject><subject>Signal Transduction</subject><subject>Vasodilation</subject><subject>Ventricular Remodeling</subject><issn>0163-7258</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtqwzAQRbVoadK0v1C06i7uSH5I7i6EviDQTZYFMZbkxsG2Ukle5O-rkEBWA3PPnYFDCGWQMWDVyz477NAPcWc9ZhygyEBmwPgNmac4Xwpeyhm5D2EPKSyA35EZKysBFWdz8rMy3o5usGbq-258pd7-Tj1G56lraTiGaIdOUxwN1ehNh5ruEu1CxNAF2o0U9RQtHY7unPdp16LXsXPjA7ltsQ_28TIXZPv-tl1_LjffH1_r1Wapc1HHZV3nnJe1KLQxrJZY1dg0kkNVouC50K1sNQAzrOGCCdZoUXIjZMEBDZSYL8jz-ezBu7_JhqiGLmjb9zhaNwVViVxCWckEyjOovQvB21YdfDegPyoG6iRT7dVVpjrJVCBVkpmqT5cfU5NkXYsXk_k_X2N3Wg</recordid><startdate>200502</startdate><enddate>200502</enddate><creator>Hamid, Shabaz A</creator><creator>Baxter, Gary F</creator><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></search><sort><creationdate>200502</creationdate><title>Adrenomedullin: regulator of systemic and cardiac homeostasis in acute myocardial infarction</title><author>Hamid, Shabaz A ; Baxter, Gary F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-993225974cdd198a69abb82065a7237cf8fc001d1b27171bc752d78420ad05a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adrenomedullin</topic><topic>Animals</topic><topic>Cell Survival</topic><topic>Coronary Vessels - metabolism</topic><topic>Coronary Vessels - physiopathology</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Inflammation Mediators - metabolism</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Oxidative Stress</topic><topic>Peptides - physiology</topic><topic>Signal Transduction</topic><topic>Vasodilation</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hamid, Shabaz A</creatorcontrib><creatorcontrib>Baxter, Gary F</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><jtitle>Pharmacology & therapeutics (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hamid, Shabaz A</au><au>Baxter, Gary F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adrenomedullin: regulator of systemic and cardiac homeostasis in acute myocardial infarction</atitle><jtitle>Pharmacology & therapeutics (Oxford)</jtitle><addtitle>Pharmacol Ther</addtitle><date>2005-02</date><risdate>2005</risdate><volume>105</volume><issue>2</issue><spage>95</spage><epage>112</epage><pages>95-112</pages><issn>0163-7258</issn><abstract>During and following acute myocardial infarction, a variety of endogenous mediators are elevated, one of which is adrenomedullin (AM). AM is a multifunctional peptide that has been identified as having a putative beneficial role following an ischemic insult at both systemic and local levels. Classically described as a potent vasodilator, natriuretic, and diuretic agent, experimental infarct models also demonstrate AM to exhibit antiproliferative and antiapoptotic functions in the myocardium, counterregulating the effects of mediators such as angiotensin-II and endothelin-1. Less well documented are the angiogenic and inflammatory modulating potentials of AM, which may also contribute toward reducing adverse ventricular remodeling. The review examines clinical and experimental studies, looking at the effects of AM and cellular mechanisms that could be involved in mediating cardioprotective effects and ultimately optimizing left ventricular remodeling. 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subjects | Adrenomedullin Animals Cell Survival Coronary Vessels - metabolism Coronary Vessels - physiopathology Homeostasis Humans Inflammation Mediators - metabolism Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - physiopathology Neovascularization, Pathologic - metabolism Oxidative Stress Peptides - physiology Signal Transduction Vasodilation Ventricular Remodeling |
title | Adrenomedullin: regulator of systemic and cardiac homeostasis in acute myocardial infarction |
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