Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction
Broad inhibition of matrix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction (MI). However, it is not clear if selective MMP inhibition strategies will be effective or if MMP inhibition will impair angiogenesis after MI. We used a selective MMP inhibitor (M...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-02, Vol.105 (6), p.753-758 |
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| creator | LINDSEY, Merry L GANNON, Joseph LEE, Richard T AIKAWA, Masanori SCHOEN, Frederick J RABKIN, Elena LOPRESTI-MORROW, Lori CRAWFORD, Jamie BLACK, Shawn LIBBY, Peter MITCHELL, Peter G |
| description | Broad inhibition of matrix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction (MI). However, it is not clear if selective MMP inhibition strategies will be effective or if MMP inhibition will impair angiogenesis after MI.
We used a selective MMP inhibitor (MMPi) that does not inhibit MMP-1 in rabbits, which, like humans but unlike rodents, express MMP-1 as a major collagenase. On day 1 after MI, rabbits were randomized to receive either inhibitor (n=10) or vehicle (n=8). At 4 weeks after MI, there were no differences in infarct size or collagen fractional area. However, MMPi reduced ventricular dilation. The increase in end-diastolic dimension from day 1 to week 4 was 3.1+/-0.5 mm for vehicle versus 1.3+/-0.3 mm for MMPi (P |
| doi_str_mv | 10.1161/hc0602.103674 |
| format | Article |
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We used a selective MMP inhibitor (MMPi) that does not inhibit MMP-1 in rabbits, which, like humans but unlike rodents, express MMP-1 as a major collagenase. On day 1 after MI, rabbits were randomized to receive either inhibitor (n=10) or vehicle (n=8). At 4 weeks after MI, there were no differences in infarct size or collagen fractional area. However, MMPi reduced ventricular dilation. The increase in end-diastolic dimension from day 1 to week 4 was 3.1+/-0.5 mm for vehicle versus 1.3+/-0.3 mm for MMPi (P<0.01). The increase in end-systolic dimension was 2.8+/-0.5 mm for vehicle and 1.3+/-0.4 mm for MMPi (P<0.05). Furthermore, MMPi reduced infarct wall thinning; the minimal infarct thickness was 0.8+/-0.1 mm for vehicle and 1.6+/-0.3 mm for MMPi (P<0.05). Interestingly, the MMPi group had increased numbers of vessels in the subendocardial layer of the infarct; the number of capillaries was increased in the subendocardial layer (46+/-4 vessels/field versus 17+/-3 vessels/field for vehicle; P<0.001), and the number of arterioles was also increased (4.0+/-0.8 vessels/field versus 2.0+/-0.4 vessels/field for vehicle; P<0.05).
MMP inhibition attenuates left ventricular remodeling even when the dominant collagenase MMP-1 is not inhibited; furthermore, this selective MMP inhibition appears to increase rather than decrease neovascularization in the subendocardium.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/hc0602.103674</identifier><identifier>PMID: 11839633</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; Cardiac Volume - drug effects ; Cardiology. Vascular system ; Collagen - metabolism ; Coronary Disease - complications ; Coronary heart disease ; Dilatation, Pathologic - diagnostic imaging ; Dilatation, Pathologic - drug therapy ; Dilatation, Pathologic - pathology ; Disease Models, Animal ; Echocardiography ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - pathology ; Enzyme Inhibitors - administration & dosage ; Enzyme Inhibitors - blood ; Halogenated Diphenyl Ethers ; Heart ; Heart Ventricles - diagnostic imaging ; Heart Ventricles - drug effects ; Heart Ventricles - pathology ; Ligation ; Male ; Matrix Metalloproteinase Inhibitors ; Medical sciences ; Myocardial Infarction - drug therapy ; Myocardial Infarction - etiology ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardium - metabolism ; Myocardium - pathology ; Neovascularization, Physiologic - drug effects ; Phenyl Ethers - administration & dosage ; Phenyl Ethers - blood ; Rabbits ; Survival Rate ; Ventricular Remodeling - drug effects</subject><ispartof>Circulation (New York, N.Y.), 2002-02, Vol.105 (6), p.753-758</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Feb 12, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-8fa2916175736c6385001446fd642797e6626fd9a882022dd7746f257d5337f03</citedby><cites>FETCH-LOGICAL-c426t-8fa2916175736c6385001446fd642797e6626fd9a882022dd7746f257d5337f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13512176$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11839633$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LINDSEY, Merry L</creatorcontrib><creatorcontrib>GANNON, Joseph</creatorcontrib><creatorcontrib>LEE, Richard T</creatorcontrib><creatorcontrib>AIKAWA, Masanori</creatorcontrib><creatorcontrib>SCHOEN, Frederick J</creatorcontrib><creatorcontrib>RABKIN, Elena</creatorcontrib><creatorcontrib>LOPRESTI-MORROW, Lori</creatorcontrib><creatorcontrib>CRAWFORD, Jamie</creatorcontrib><creatorcontrib>BLACK, Shawn</creatorcontrib><creatorcontrib>LIBBY, Peter</creatorcontrib><creatorcontrib>MITCHELL, Peter G</creatorcontrib><title>Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Broad inhibition of matrix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction (MI). However, it is not clear if selective MMP inhibition strategies will be effective or if MMP inhibition will impair angiogenesis after MI.
We used a selective MMP inhibitor (MMPi) that does not inhibit MMP-1 in rabbits, which, like humans but unlike rodents, express MMP-1 as a major collagenase. On day 1 after MI, rabbits were randomized to receive either inhibitor (n=10) or vehicle (n=8). At 4 weeks after MI, there were no differences in infarct size or collagen fractional area. However, MMPi reduced ventricular dilation. The increase in end-diastolic dimension from day 1 to week 4 was 3.1+/-0.5 mm for vehicle versus 1.3+/-0.3 mm for MMPi (P<0.01). The increase in end-systolic dimension was 2.8+/-0.5 mm for vehicle and 1.3+/-0.4 mm for MMPi (P<0.05). Furthermore, MMPi reduced infarct wall thinning; the minimal infarct thickness was 0.8+/-0.1 mm for vehicle and 1.6+/-0.3 mm for MMPi (P<0.05). Interestingly, the MMPi group had increased numbers of vessels in the subendocardial layer of the infarct; the number of capillaries was increased in the subendocardial layer (46+/-4 vessels/field versus 17+/-3 vessels/field for vehicle; P<0.001), and the number of arterioles was also increased (4.0+/-0.8 vessels/field versus 2.0+/-0.4 vessels/field for vehicle; P<0.05).
MMP inhibition attenuates left ventricular remodeling even when the dominant collagenase MMP-1 is not inhibited; furthermore, this selective MMP inhibition appears to increase rather than decrease neovascularization in the subendocardium.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cardiac Volume - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Collagen - metabolism</subject><subject>Coronary Disease - complications</subject><subject>Coronary heart disease</subject><subject>Dilatation, Pathologic - diagnostic imaging</subject><subject>Dilatation, Pathologic - drug therapy</subject><subject>Dilatation, Pathologic - pathology</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - pathology</subject><subject>Enzyme Inhibitors - administration & dosage</subject><subject>Enzyme Inhibitors - blood</subject><subject>Halogenated Diphenyl Ethers</subject><subject>Heart</subject><subject>Heart Ventricles - diagnostic imaging</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - pathology</subject><subject>Ligation</subject><subject>Male</subject><subject>Matrix Metalloproteinase Inhibitors</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Phenyl Ethers - administration & dosage</subject><subject>Phenyl Ethers - blood</subject><subject>Rabbits</subject><subject>Survival Rate</subject><subject>Ventricular Remodeling - drug effects</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0c9LHDEUB_BQWupWe-y1hEJ7G82PSTJzFKlWEDyo5yGbvKyRTKJJRvSv6L9slt0i9BQe7_NeEr4IfaPkmFJJT-4NkYQdU8Kl6j-gFRWs73rBx49oRQgZO8UZO0BfSnlopeRKfEYHlA58lJyv0N8bCGCqfwY865r9C56h6hDSY04VfNQFsI_3fu2rTxFnsIuBggO4ip8htgmzBJ1bY04Wgo8bvF4qtqmhmOq_WazjxqcNRCi-YO0qZDy_JqOz9To05XQ22xuO0CenQ4Gv-_MQ3Z3_vj37011dX1yenV51pmeydoPTbGzfV0JxaSQfBCG076WzsmdqVCAla8Woh4ERxqxVqjWZUFZwrhzhh-jXbm_759MCpU6zLwZC0BHSUiZFezFytoU__oMPacmxvW1ilCkmFVUNdTtkciolg5ses591fp0ombYxTbuYpl1MzX_fL13WM9h3vc-lgZ97oIvRwWUdjS_vjgvKqJL8DRDVnCs</recordid><startdate>20020212</startdate><enddate>20020212</enddate><creator>LINDSEY, Merry L</creator><creator>GANNON, Joseph</creator><creator>LEE, Richard T</creator><creator>AIKAWA, Masanori</creator><creator>SCHOEN, Frederick J</creator><creator>RABKIN, Elena</creator><creator>LOPRESTI-MORROW, Lori</creator><creator>CRAWFORD, Jamie</creator><creator>BLACK, Shawn</creator><creator>LIBBY, Peter</creator><creator>MITCHELL, Peter G</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20020212</creationdate><title>Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction</title><author>LINDSEY, Merry L ; GANNON, Joseph ; LEE, Richard T ; AIKAWA, Masanori ; SCHOEN, Frederick J ; RABKIN, Elena ; LOPRESTI-MORROW, Lori ; CRAWFORD, Jamie ; BLACK, Shawn ; LIBBY, Peter ; MITCHELL, Peter G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-8fa2916175736c6385001446fd642797e6626fd9a882022dd7746f257d5337f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cardiac Volume - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Collagen - metabolism</topic><topic>Coronary Disease - complications</topic><topic>Coronary heart disease</topic><topic>Dilatation, Pathologic - diagnostic imaging</topic><topic>Dilatation, Pathologic - drug therapy</topic><topic>Dilatation, Pathologic - pathology</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - pathology</topic><topic>Enzyme Inhibitors - administration & dosage</topic><topic>Enzyme Inhibitors - blood</topic><topic>Halogenated Diphenyl Ethers</topic><topic>Heart</topic><topic>Heart Ventricles - diagnostic imaging</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - pathology</topic><topic>Ligation</topic><topic>Male</topic><topic>Matrix Metalloproteinase Inhibitors</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Phenyl Ethers - administration & dosage</topic><topic>Phenyl Ethers - blood</topic><topic>Rabbits</topic><topic>Survival Rate</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LINDSEY, Merry L</creatorcontrib><creatorcontrib>GANNON, Joseph</creatorcontrib><creatorcontrib>LEE, Richard T</creatorcontrib><creatorcontrib>AIKAWA, Masanori</creatorcontrib><creatorcontrib>SCHOEN, Frederick J</creatorcontrib><creatorcontrib>RABKIN, Elena</creatorcontrib><creatorcontrib>LOPRESTI-MORROW, Lori</creatorcontrib><creatorcontrib>CRAWFORD, Jamie</creatorcontrib><creatorcontrib>BLACK, Shawn</creatorcontrib><creatorcontrib>LIBBY, Peter</creatorcontrib><creatorcontrib>MITCHELL, Peter G</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LINDSEY, Merry L</au><au>GANNON, Joseph</au><au>LEE, Richard T</au><au>AIKAWA, Masanori</au><au>SCHOEN, Frederick J</au><au>RABKIN, Elena</au><au>LOPRESTI-MORROW, Lori</au><au>CRAWFORD, Jamie</au><au>BLACK, Shawn</au><au>LIBBY, Peter</au><au>MITCHELL, Peter G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-02-12</date><risdate>2002</risdate><volume>105</volume><issue>6</issue><spage>753</spage><epage>758</epage><pages>753-758</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Broad inhibition of matrix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction (MI). However, it is not clear if selective MMP inhibition strategies will be effective or if MMP inhibition will impair angiogenesis after MI.
We used a selective MMP inhibitor (MMPi) that does not inhibit MMP-1 in rabbits, which, like humans but unlike rodents, express MMP-1 as a major collagenase. On day 1 after MI, rabbits were randomized to receive either inhibitor (n=10) or vehicle (n=8). At 4 weeks after MI, there were no differences in infarct size or collagen fractional area. However, MMPi reduced ventricular dilation. The increase in end-diastolic dimension from day 1 to week 4 was 3.1+/-0.5 mm for vehicle versus 1.3+/-0.3 mm for MMPi (P<0.01). The increase in end-systolic dimension was 2.8+/-0.5 mm for vehicle and 1.3+/-0.4 mm for MMPi (P<0.05). Furthermore, MMPi reduced infarct wall thinning; the minimal infarct thickness was 0.8+/-0.1 mm for vehicle and 1.6+/-0.3 mm for MMPi (P<0.05). Interestingly, the MMPi group had increased numbers of vessels in the subendocardial layer of the infarct; the number of capillaries was increased in the subendocardial layer (46+/-4 vessels/field versus 17+/-3 vessels/field for vehicle; P<0.001), and the number of arterioles was also increased (4.0+/-0.8 vessels/field versus 2.0+/-0.4 vessels/field for vehicle; P<0.05).
MMP inhibition attenuates left ventricular remodeling even when the dominant collagenase MMP-1 is not inhibited; furthermore, this selective MMP inhibition appears to increase rather than decrease neovascularization in the subendocardium.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11839633</pmid><doi>10.1161/hc0602.103674</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Blotting, Western Cardiac Volume - drug effects Cardiology. Vascular system Collagen - metabolism Coronary Disease - complications Coronary heart disease Dilatation, Pathologic - diagnostic imaging Dilatation, Pathologic - drug therapy Dilatation, Pathologic - pathology Disease Models, Animal Echocardiography Endothelium, Vascular - drug effects Endothelium, Vascular - pathology Enzyme Inhibitors - administration & dosage Enzyme Inhibitors - blood Halogenated Diphenyl Ethers Heart Heart Ventricles - diagnostic imaging Heart Ventricles - drug effects Heart Ventricles - pathology Ligation Male Matrix Metalloproteinase Inhibitors Medical sciences Myocardial Infarction - drug therapy Myocardial Infarction - etiology Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium - metabolism Myocardium - pathology Neovascularization, Physiologic - drug effects Phenyl Ethers - administration & dosage Phenyl Ethers - blood Rabbits Survival Rate Ventricular Remodeling - drug effects |
| title | Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction |
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