Oxidative stress and inflammation in heart failure: mechanisms of damage and therapeutic alternatives
Despite advances in treatment, chronic heart failure still is associated with a poor prognosis and remains a leading cause of cardiovascular death. Cumulating evidence suggests that imbalances in redox state lead to a higher generation of reactive oxygen species. This phenomenon, along with pro-infl...
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| Veröffentlicht in: | Revista medíca de Chile 2007-08, Vol.135 (8), p.1056 |
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| container_title | Revista medíca de Chile |
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| creator | Miranda H, Rodrigo Castro G, Pablo Verdejo P, Hugo Chiong, Mario Díaz-Araya, Guillermo Mellado, Rosemarie Rojas, Diego Concepción, Roberto Lavandera, Sergio |
| description | Despite advances in treatment, chronic heart failure still is associated with a poor prognosis and remains a leading cause of cardiovascular death. Cumulating evidence suggests that imbalances in redox state lead to a higher generation of reactive oxygen species. This phenomenon, along with pro-inflammatory cytokine activation and extra cellular matrix alterations with reactive fibrosis, play an important role in the pathogenesis and progression of heart failure, through the development of endothelial and myocardial dysfunction. The understanding of the underlying phenomena and the metabolic pathways involved will allow further development of therapies aiming to change the natural history of heart failure. |
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The understanding of the underlying phenomena and the metabolic pathways involved will allow further development of therapies aiming to change the natural history of heart failure.</description><identifier>ISSN: 0034-9887</identifier><identifier>PMID: 17989865</identifier><language>spa</language><publisher>Chile</publisher><subject>Animals ; Disease Models, Animal ; Endothelium, Vascular - physiopathology ; Evidence-Based Medicine ; Heart Failure - physiopathology ; Heart Failure - therapy ; Humans ; Inflammation - physiopathology ; Metalloproteases - analysis ; Metalloproteases - physiology ; Oxidative Stress - physiology</subject><ispartof>Revista medíca de Chile, 2007-08, Vol.135 (8), p.1056</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17989865$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miranda H, Rodrigo</creatorcontrib><creatorcontrib>Castro G, Pablo</creatorcontrib><creatorcontrib>Verdejo P, Hugo</creatorcontrib><creatorcontrib>Chiong, Mario</creatorcontrib><creatorcontrib>Díaz-Araya, Guillermo</creatorcontrib><creatorcontrib>Mellado, Rosemarie</creatorcontrib><creatorcontrib>Rojas, Diego</creatorcontrib><creatorcontrib>Concepción, Roberto</creatorcontrib><creatorcontrib>Lavandera, Sergio</creatorcontrib><title>Oxidative stress and inflammation in heart failure: mechanisms of damage and therapeutic alternatives</title><title>Revista medíca de Chile</title><addtitle>Rev Med Chil</addtitle><description>Despite advances in treatment, chronic heart failure still is associated with a poor prognosis and remains a leading cause of cardiovascular death. Cumulating evidence suggests that imbalances in redox state lead to a higher generation of reactive oxygen species. This phenomenon, along with pro-inflammatory cytokine activation and extra cellular matrix alterations with reactive fibrosis, play an important role in the pathogenesis and progression of heart failure, through the development of endothelial and myocardial dysfunction. The understanding of the underlying phenomena and the metabolic pathways involved will allow further development of therapies aiming to change the natural history of heart failure.</description><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Evidence-Based Medicine</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - therapy</subject><subject>Humans</subject><subject>Inflammation - physiopathology</subject><subject>Metalloproteases - analysis</subject><subject>Metalloproteases - physiology</subject><subject>Oxidative Stress - physiology</subject><issn>0034-9887</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j81KAzEUhbNQbK19BckLDCSTzEziTop_UOhG1-UmuelEJtMhyYi-vaXa1eEc-D44V2TJmJCVVqpbkNucPxmru5arG7LgnVZatc2S4O47OCjhC2kuCXOmMDoaRj9AjKf9OJ4K7RFSoR7CMCd8oBFtD2PIMdOjpw4iHPDMlR4TTDiXYCkMBdN4Vuc7cu1hyLj-zxX5eH5637xW293L2-ZxW02cqVJJ5rU1tWkk18a2jeEOTG1BqLrmmnPtDTcAjVfMCKelbaXlyBgy3wEYJ1bk_s87zSai208pREg_-8tf8Qv041OS</recordid><startdate>200708</startdate><enddate>200708</enddate><creator>Miranda H, Rodrigo</creator><creator>Castro G, Pablo</creator><creator>Verdejo P, Hugo</creator><creator>Chiong, Mario</creator><creator>Díaz-Araya, Guillermo</creator><creator>Mellado, Rosemarie</creator><creator>Rojas, Diego</creator><creator>Concepción, Roberto</creator><creator>Lavandera, Sergio</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>200708</creationdate><title>Oxidative stress and inflammation in heart failure: mechanisms of damage and therapeutic alternatives</title><author>Miranda H, Rodrigo ; Castro G, Pablo ; Verdejo P, Hugo ; Chiong, Mario ; Díaz-Araya, Guillermo ; Mellado, Rosemarie ; Rojas, Diego ; Concepción, Roberto ; Lavandera, Sergio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p108t-40f9cb2b5419bc65b1dab2ca382219119fb1baa5f80b3d94c64c1e00e0f7aabd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>spa</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Evidence-Based Medicine</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - therapy</topic><topic>Humans</topic><topic>Inflammation - physiopathology</topic><topic>Metalloproteases - analysis</topic><topic>Metalloproteases - physiology</topic><topic>Oxidative Stress - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miranda H, Rodrigo</creatorcontrib><creatorcontrib>Castro G, Pablo</creatorcontrib><creatorcontrib>Verdejo P, Hugo</creatorcontrib><creatorcontrib>Chiong, Mario</creatorcontrib><creatorcontrib>Díaz-Araya, Guillermo</creatorcontrib><creatorcontrib>Mellado, Rosemarie</creatorcontrib><creatorcontrib>Rojas, Diego</creatorcontrib><creatorcontrib>Concepción, Roberto</creatorcontrib><creatorcontrib>Lavandera, Sergio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Revista medíca de Chile</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miranda H, Rodrigo</au><au>Castro G, Pablo</au><au>Verdejo P, Hugo</au><au>Chiong, Mario</au><au>Díaz-Araya, Guillermo</au><au>Mellado, Rosemarie</au><au>Rojas, Diego</au><au>Concepción, Roberto</au><au>Lavandera, Sergio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress and inflammation in heart failure: mechanisms of damage and therapeutic alternatives</atitle><jtitle>Revista medíca de Chile</jtitle><addtitle>Rev Med Chil</addtitle><date>2007-08</date><risdate>2007</risdate><volume>135</volume><issue>8</issue><spage>1056</spage><pages>1056-</pages><issn>0034-9887</issn><abstract>Despite advances in treatment, chronic heart failure still is associated with a poor prognosis and remains a leading cause of cardiovascular death. Cumulating evidence suggests that imbalances in redox state lead to a higher generation of reactive oxygen species. This phenomenon, along with pro-inflammatory cytokine activation and extra cellular matrix alterations with reactive fibrosis, play an important role in the pathogenesis and progression of heart failure, through the development of endothelial and myocardial dysfunction. The understanding of the underlying phenomena and the metabolic pathways involved will allow further development of therapies aiming to change the natural history of heart failure.</abstract><cop>Chile</cop><pmid>17989865</pmid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0034-9887 |
| ispartof | Revista medíca de Chile, 2007-08, Vol.135 (8), p.1056 |
| issn | 0034-9887 |
| language | spa |
| recordid | cdi_pubmed_primary_17989865 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Disease Models, Animal Endothelium, Vascular - physiopathology Evidence-Based Medicine Heart Failure - physiopathology Heart Failure - therapy Humans Inflammation - physiopathology Metalloproteases - analysis Metalloproteases - physiology Oxidative Stress - physiology |
| title | Oxidative stress and inflammation in heart failure: mechanisms of damage and therapeutic alternatives |
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