Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart
Cardiac hypertrophy is an adaptive response to increased workload that, if unrelieved, leads to heart failure. It has been reported that cardiomyocyte apoptosis contributes to failure, and that vascular endothelial growth factor (VEGF) treatment of hypertrophied myocardium increases capillary densit...
Gespeichert in:
| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2006-07, Vol.114 (1), p.I290-I295 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | I295 |
|---|---|
| container_issue | 1 |
| container_start_page | I290 |
| container_title | Circulation (New York, N.Y.) |
| container_volume | 114 |
| creator | FRIEHS, Ingeborg BARILLAS, Rodrigo VASILYEV, Nikolay V ROY, Nathalie MCGOWAN, Francis X DEL NIDO, Pedro J |
| description | Cardiac hypertrophy is an adaptive response to increased workload that, if unrelieved, leads to heart failure. It has been reported that cardiomyocyte apoptosis contributes to failure, and that vascular endothelial growth factor (VEGF) treatment of hypertrophied myocardium increases capillary density and improves myocardial perfusion. In this study we hypothesized that VEGF treatment reduces cardiomyocyte apoptosis and thereby preserves myocardial contractile function.
Newborn rabbits underwent aortic banding. At 4 and 6 weeks of age, hypertrophied animals were treated with intrapericardial administration of recombinant VEGF protein. Three groups of animals were investigated: age-matched controls (C), untreated hypertrophied (H), and VEGF-treated hypertrophied hearts (T). Cardiomyocyte apoptosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and cardiac function by transthoracic echocardiography. Death attributable to severe heart failure occurred in 14 of 43 untreated and 2 of 29 VEGF-treated animals (P |
| doi_str_mv | 10.1161/circulationaha.105.001289 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3444258</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68604909</sourcerecordid><originalsourceid>FETCH-LOGICAL-c566t-2678de7ee53c1658162c376e5cd0b099d11559b243d25e32937e133590aba1ee3</originalsourceid><addsrcrecordid>eNpVkV2L1DAYhYMo7rj6FyRe6F3HfDRpcyMMg7oDgwuy623IpG-3kU5Sk3Rk_70pM7gKgSQnz3ty4CD0jpI1pZJ-tC7aeTTZBW8Gs6ZErAmhrFXP0IoKVle14Oo5WhFCVNVwxq7Qq5R-lqvkjXiJrqhsGRFtu0KnHyYtXhGD70IeYHRmxA8x_M4D7o3NIeIpwgl8TthMYcohuXLy3SIniCdI2AafY2HdCLifvV2CYefx8DhBzDFMg4OuCL3xGQ9gYn6NXvRmTPDmsl-j-y-f77Y31f7262672VdWSJkrJpu2gwZAcEulaKlkljcShO3IgSjVUSqEOrCad0wAZ4o3QDkXipiDoQD8Gn06-07z4QidhSXoqKfojiY-6mCc_v_Fu0E_hJPmdV0z0RaDDxeDGH7NkLI-umRhHI2HMCctW0lqRVQB1Rm0MaQUof_7CSV6aU1vd9-39_vN3e722-ZmU2Shz62V2bf_pnyavNRUgPcXoLRlxj4ab1164hpVt7ysP1HxqAE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68604909</pqid></control><display><type>article</type><title>Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Journals@Ovid Complete</source><creator>FRIEHS, Ingeborg ; BARILLAS, Rodrigo ; VASILYEV, Nikolay V ; ROY, Nathalie ; MCGOWAN, Francis X ; DEL NIDO, Pedro J</creator><creatorcontrib>FRIEHS, Ingeborg ; BARILLAS, Rodrigo ; VASILYEV, Nikolay V ; ROY, Nathalie ; MCGOWAN, Francis X ; DEL NIDO, Pedro J</creatorcontrib><description>Cardiac hypertrophy is an adaptive response to increased workload that, if unrelieved, leads to heart failure. It has been reported that cardiomyocyte apoptosis contributes to failure, and that vascular endothelial growth factor (VEGF) treatment of hypertrophied myocardium increases capillary density and improves myocardial perfusion. In this study we hypothesized that VEGF treatment reduces cardiomyocyte apoptosis and thereby preserves myocardial contractile function.
Newborn rabbits underwent aortic banding. At 4 and 6 weeks of age, hypertrophied animals were treated with intrapericardial administration of recombinant VEGF protein. Three groups of animals were investigated: age-matched controls (C), untreated hypertrophied (H), and VEGF-treated hypertrophied hearts (T). Cardiomyocyte apoptosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and cardiac function by transthoracic echocardiography. Death attributable to severe heart failure occurred in 14 of 43 untreated and 2 of 29 VEGF-treated animals (P<0.01). TUNEL-positive cardiomyocyte nuclei (n/1000 nuclei) were significantly increased in untreated hearts at 5 weeks (H: 10+/-1.8 versus T: 3+/-0.7) and at 7 weeks (H: 13+/-3.6 versus T: 5+/-1.5; P<0.05). Increased apoptosis in untreated hypertrophy was also confirmed by the presence of PARP cleavage (H: 74+/-7 versus T: 41+/-4 arbitrary densitometry units; P<0.05). VEGF treatment preserved left ventricular mass, prevented dilation (T: 1.01+/-0.06 versus H: 0.77+/-0.07; P<0.05), and preserved contractility indices compared with untreated hearts.
Lack of adaptive capillary growth impairs myocardial perfusion and substrate delivery in hypertrophying myocardium. VEGF treatment reduces myocardial apoptosis and prolongs survival in a model of severe progressive left ventricular hypertrophy. Promoting capillary growth with VEGF reduces apoptosis, preserves myocardial contractile function, and delays the onset of failure in pressure-loaded infant myocardium.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/circulationaha.105.001289</identifier><identifier>PMID: 16820588</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Animals, Newborn ; Aorta, Thoracic ; Apoptosis - drug effects ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Capillaries - drug effects ; Cardiology. Vascular system ; Cardiomyopathy, Hypertrophic - drug therapy ; Cardiomyopathy, Hypertrophic - etiology ; Cardiomyopathy, Hypertrophic - pathology ; Cardiomyopathy, Hypertrophic - physiopathology ; Coronary heart disease ; Disease Progression ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Drug Evaluation, Preclinical ; Fundamental and applied biological sciences. Psychology ; Heart ; Hypertrophy, Left Ventricular - drug therapy ; Hypertrophy, Left Ventricular - etiology ; Hypertrophy, Left Ventricular - pathology ; Hypertrophy, Left Ventricular - physiopathology ; In Situ Nick-End Labeling ; Ligation ; Medical sciences ; Myocardial Contraction - drug effects ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - pathology ; Neovascularization, Physiologic - drug effects ; Poly(ADP-ribose) Polymerases - metabolism ; Rabbits ; Recombinant Proteins - therapeutic use ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - therapeutic use ; Vertebrates: cardiovascular system</subject><ispartof>Circulation (New York, N.Y.), 2006-07, Vol.114 (1), p.I290-I295</ispartof><rights>2006 INIST-CNRS</rights><rights>2006 American Heart Association, Inc. 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c566t-2678de7ee53c1658162c376e5cd0b099d11559b243d25e32937e133590aba1ee3</citedby><cites>FETCH-LOGICAL-c566t-2678de7ee53c1658162c376e5cd0b099d11559b243d25e32937e133590aba1ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,309,310,314,780,784,789,790,885,3687,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17948348$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16820588$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FRIEHS, Ingeborg</creatorcontrib><creatorcontrib>BARILLAS, Rodrigo</creatorcontrib><creatorcontrib>VASILYEV, Nikolay V</creatorcontrib><creatorcontrib>ROY, Nathalie</creatorcontrib><creatorcontrib>MCGOWAN, Francis X</creatorcontrib><creatorcontrib>DEL NIDO, Pedro J</creatorcontrib><title>Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Cardiac hypertrophy is an adaptive response to increased workload that, if unrelieved, leads to heart failure. It has been reported that cardiomyocyte apoptosis contributes to failure, and that vascular endothelial growth factor (VEGF) treatment of hypertrophied myocardium increases capillary density and improves myocardial perfusion. In this study we hypothesized that VEGF treatment reduces cardiomyocyte apoptosis and thereby preserves myocardial contractile function.
Newborn rabbits underwent aortic banding. At 4 and 6 weeks of age, hypertrophied animals were treated with intrapericardial administration of recombinant VEGF protein. Three groups of animals were investigated: age-matched controls (C), untreated hypertrophied (H), and VEGF-treated hypertrophied hearts (T). Cardiomyocyte apoptosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and cardiac function by transthoracic echocardiography. Death attributable to severe heart failure occurred in 14 of 43 untreated and 2 of 29 VEGF-treated animals (P<0.01). TUNEL-positive cardiomyocyte nuclei (n/1000 nuclei) were significantly increased in untreated hearts at 5 weeks (H: 10+/-1.8 versus T: 3+/-0.7) and at 7 weeks (H: 13+/-3.6 versus T: 5+/-1.5; P<0.05). Increased apoptosis in untreated hypertrophy was also confirmed by the presence of PARP cleavage (H: 74+/-7 versus T: 41+/-4 arbitrary densitometry units; P<0.05). VEGF treatment preserved left ventricular mass, prevented dilation (T: 1.01+/-0.06 versus H: 0.77+/-0.07; P<0.05), and preserved contractility indices compared with untreated hearts.
Lack of adaptive capillary growth impairs myocardial perfusion and substrate delivery in hypertrophying myocardium. VEGF treatment reduces myocardial apoptosis and prolongs survival in a model of severe progressive left ventricular hypertrophy. Promoting capillary growth with VEGF reduces apoptosis, preserves myocardial contractile function, and delays the onset of failure in pressure-loaded infant myocardium.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Aorta, Thoracic</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Capillaries - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomyopathy, Hypertrophic - drug therapy</subject><subject>Cardiomyopathy, Hypertrophic - etiology</subject><subject>Cardiomyopathy, Hypertrophic - pathology</subject><subject>Cardiomyopathy, Hypertrophic - physiopathology</subject><subject>Coronary heart disease</subject><subject>Disease Progression</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Drug Evaluation, Preclinical</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Hypertrophy, Left Ventricular - drug therapy</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Hypertrophy, Left Ventricular - physiopathology</subject><subject>In Situ Nick-End Labeling</subject><subject>Ligation</subject><subject>Medical sciences</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Rabbits</subject><subject>Recombinant Proteins - therapeutic use</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - therapeutic use</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkV2L1DAYhYMo7rj6FyRe6F3HfDRpcyMMg7oDgwuy623IpG-3kU5Sk3Rk_70pM7gKgSQnz3ty4CD0jpI1pZJ-tC7aeTTZBW8Gs6ZErAmhrFXP0IoKVle14Oo5WhFCVNVwxq7Qq5R-lqvkjXiJrqhsGRFtu0KnHyYtXhGD70IeYHRmxA8x_M4D7o3NIeIpwgl8TthMYcohuXLy3SIniCdI2AafY2HdCLifvV2CYefx8DhBzDFMg4OuCL3xGQ9gYn6NXvRmTPDmsl-j-y-f77Y31f7262672VdWSJkrJpu2gwZAcEulaKlkljcShO3IgSjVUSqEOrCad0wAZ4o3QDkXipiDoQD8Gn06-07z4QidhSXoqKfojiY-6mCc_v_Fu0E_hJPmdV0z0RaDDxeDGH7NkLI-umRhHI2HMCctW0lqRVQB1Rm0MaQUof_7CSV6aU1vd9-39_vN3e722-ZmU2Shz62V2bf_pnyavNRUgPcXoLRlxj4ab1164hpVt7ysP1HxqAE</recordid><startdate>20060704</startdate><enddate>20060704</enddate><creator>FRIEHS, Ingeborg</creator><creator>BARILLAS, Rodrigo</creator><creator>VASILYEV, Nikolay V</creator><creator>ROY, Nathalie</creator><creator>MCGOWAN, Francis X</creator><creator>DEL NIDO, Pedro J</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><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>20060704</creationdate><title>Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart</title><author>FRIEHS, Ingeborg ; BARILLAS, Rodrigo ; VASILYEV, Nikolay V ; ROY, Nathalie ; MCGOWAN, Francis X ; DEL NIDO, Pedro J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c566t-2678de7ee53c1658162c376e5cd0b099d11559b243d25e32937e133590aba1ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Aorta, Thoracic</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Capillaries - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomyopathy, Hypertrophic - drug therapy</topic><topic>Cardiomyopathy, Hypertrophic - etiology</topic><topic>Cardiomyopathy, Hypertrophic - pathology</topic><topic>Cardiomyopathy, Hypertrophic - physiopathology</topic><topic>Coronary heart disease</topic><topic>Disease Progression</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Drug Evaluation, Preclinical</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Hypertrophy, Left Ventricular - drug therapy</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Hypertrophy, Left Ventricular - physiopathology</topic><topic>In Situ Nick-End Labeling</topic><topic>Ligation</topic><topic>Medical sciences</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Rabbits</topic><topic>Recombinant Proteins - therapeutic use</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - therapeutic use</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FRIEHS, Ingeborg</creatorcontrib><creatorcontrib>BARILLAS, Rodrigo</creatorcontrib><creatorcontrib>VASILYEV, Nikolay V</creatorcontrib><creatorcontrib>ROY, Nathalie</creatorcontrib><creatorcontrib>MCGOWAN, Francis X</creatorcontrib><creatorcontrib>DEL NIDO, Pedro J</creatorcontrib><collection>Pascal-Francis</collection><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>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FRIEHS, Ingeborg</au><au>BARILLAS, Rodrigo</au><au>VASILYEV, Nikolay V</au><au>ROY, Nathalie</au><au>MCGOWAN, Francis X</au><au>DEL NIDO, Pedro J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2006-07-04</date><risdate>2006</risdate><volume>114</volume><issue>1</issue><spage>I290</spage><epage>I295</epage><pages>I290-I295</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Cardiac hypertrophy is an adaptive response to increased workload that, if unrelieved, leads to heart failure. It has been reported that cardiomyocyte apoptosis contributes to failure, and that vascular endothelial growth factor (VEGF) treatment of hypertrophied myocardium increases capillary density and improves myocardial perfusion. In this study we hypothesized that VEGF treatment reduces cardiomyocyte apoptosis and thereby preserves myocardial contractile function.
Newborn rabbits underwent aortic banding. At 4 and 6 weeks of age, hypertrophied animals were treated with intrapericardial administration of recombinant VEGF protein. Three groups of animals were investigated: age-matched controls (C), untreated hypertrophied (H), and VEGF-treated hypertrophied hearts (T). Cardiomyocyte apoptosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and cardiac function by transthoracic echocardiography. Death attributable to severe heart failure occurred in 14 of 43 untreated and 2 of 29 VEGF-treated animals (P<0.01). TUNEL-positive cardiomyocyte nuclei (n/1000 nuclei) were significantly increased in untreated hearts at 5 weeks (H: 10+/-1.8 versus T: 3+/-0.7) and at 7 weeks (H: 13+/-3.6 versus T: 5+/-1.5; P<0.05). Increased apoptosis in untreated hypertrophy was also confirmed by the presence of PARP cleavage (H: 74+/-7 versus T: 41+/-4 arbitrary densitometry units; P<0.05). VEGF treatment preserved left ventricular mass, prevented dilation (T: 1.01+/-0.06 versus H: 0.77+/-0.07; P<0.05), and preserved contractility indices compared with untreated hearts.
Lack of adaptive capillary growth impairs myocardial perfusion and substrate delivery in hypertrophying myocardium. VEGF treatment reduces myocardial apoptosis and prolongs survival in a model of severe progressive left ventricular hypertrophy. Promoting capillary growth with VEGF reduces apoptosis, preserves myocardial contractile function, and delays the onset of failure in pressure-loaded infant myocardium.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>16820588</pmid><doi>10.1161/circulationaha.105.001289</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-7322 |
| ispartof | Circulation (New York, N.Y.), 2006-07, Vol.114 (1), p.I290-I295 |
| issn | 0009-7322 1524-4539 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3444258 |
| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Animals Animals, Newborn Aorta, Thoracic Apoptosis - drug effects Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Capillaries - drug effects Cardiology. Vascular system Cardiomyopathy, Hypertrophic - drug therapy Cardiomyopathy, Hypertrophic - etiology Cardiomyopathy, Hypertrophic - pathology Cardiomyopathy, Hypertrophic - physiopathology Coronary heart disease Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Drug Evaluation, Preclinical Fundamental and applied biological sciences. Psychology Heart Hypertrophy, Left Ventricular - drug therapy Hypertrophy, Left Ventricular - etiology Hypertrophy, Left Ventricular - pathology Hypertrophy, Left Ventricular - physiopathology In Situ Nick-End Labeling Ligation Medical sciences Myocardial Contraction - drug effects Myocytes, Cardiac - drug effects Myocytes, Cardiac - pathology Neovascularization, Physiologic - drug effects Poly(ADP-ribose) Polymerases - metabolism Rabbits Recombinant Proteins - therapeutic use Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - therapeutic use Vertebrates: cardiovascular system |
| title | Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T23%3A17%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Vascular%20endothelial%20growth%20factor%20prevents%20apoptosis%20and%20preserves%20contractile%20function%20in%20hypertrophied%20infant%20heart&rft.jtitle=Circulation%20(New%20York,%20N.Y.)&rft.au=FRIEHS,%20Ingeborg&rft.date=2006-07-04&rft.volume=114&rft.issue=1&rft.spage=I290&rft.epage=I295&rft.pages=I290-I295&rft.issn=0009-7322&rft.eissn=1524-4539&rft.coden=CIRCAZ&rft_id=info:doi/10.1161/circulationaha.105.001289&rft_dat=%3Cproquest_pubme%3E68604909%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=68604909&rft_id=info:pmid/16820588&rfr_iscdi=true |