Matrix metalloproteinases and cardiovascular diseases

The paper reviews the role of matrix metalloproteinases of proteolytic system that perform a great variety of function and control almost all biological processes. According to the classification all proteases are divided into four families serine, cysteine, aspartate and metalloproteinases (last also called matrix metalloproteinases (MMP)). Up to now 28 MMP are known (from MMP-1 to MMP-28). Based on structural features and substrate specificity MMP family was divided into identified 4 subfamilies: collagenases, gelatinases. stromelizines and unclassified MMP. Study of MMP family in cardiology significantly expands the understanding of the pathogenetic mechanisms of cardiovascular diseases and demonstrates different MMPs functions: stromelizine MMP-3, collagenase - MMP-8, gelatinase - MMP-9. It is assumed that MMP-3 and MMP-9 play an important role in acute myocardial infarction, unstable angina, rehabilitation after a heart attack, left ventricular remodeling. There are data of special role of MMP-3, MMP-9 gene polymorphism associated with susceptibility to cardiovascular disease, atherosclerosis of the arteries, heart attack, aneurysm of the aorta. However, role of MMP-2, MMP-7 and unclassified MMPs in cardiac pathology is not well investigated and remains controversial.

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THE ROLE OF MATRIX METALLOPROTEINASES IN LEFT VENTRICULAR REMODELING IN PATIENTS WITH ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION

Fundamental and Clinical Medicine ◽

10.23946/2500-0764-2019-4-2-28-41 ◽

2019 ◽

Vol 4 (2) ◽

pp. 28-41

Author(s):

TAMARA B. PECHERINA ◽

◽

OLGA V. GRUZDEVA ◽

OLGA L. BARBARASH ◽

◽

...

Keyword(s):

Myocardial Infarction ◽

Matrix Metalloproteinases ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

St Segment Elevation ◽

Segment Elevation Myocardial Infarction ◽

St Segment

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Faculty Opinions recommendation of Critical role of the NAD(P)H oxidase subunit p47phox for left ventricular remodeling/dysfunction and survival after myocardial infarction.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1081843.534768 ◽

2007 ◽

Author(s):

Fabio Recchia

Keyword(s):

Myocardial Infarction ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Critical Role ◽

Left Ventricular ◽

Oxidase Subunit

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Faculty Opinions recommendation of Regulatory role of dendritic cells in postinfarction healing and left ventricular remodeling.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.716447800.791852800 ◽

2012 ◽

Author(s):

David Kluth ◽

Neeraj Dhaun

Keyword(s):

Dendritic Cells ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

Regulatory Role

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Role of oxidative stress in left ventricular remodeling and heart failure after myocardial infarction

Journal of Cardiac Failure ◽

10.1016/s1071-9164(99)91277-0 ◽

1999 ◽

Vol 5 (3) ◽

pp. 79

Author(s):

Shintaro Kinugawa ◽

Hiroyuki Tsutsui ◽

Tomomi Ide ◽

Hideo Ustumi ◽

Nobuhiro Suematsu ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Heart Failure ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular

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Abstract 865: Gata-4 Is An Angiogenic Survival Factor Of The Infarcted Heart

Circulation ◽

10.1161/circ.116.suppl_16.ii_169 ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Olli Tenhunen ◽

Hanna Leskinen ◽

Raisa Serpi ◽

Jaana Rysä ◽

Harri Pennanen ◽

...

Keyword(s):

Heart Failure ◽

Stem Cells ◽

Gene Transfer ◽

Dna Binding ◽

Ventricular Remodeling ◽

Left Ventricular Remodeling ◽

Left Ventricular ◽

Therapeutic Interventions ◽

Cardiac Stem Cells

Recent data suggest that the cardiac-restricted transcription factor GATA-4 is an anti-apoptotic factor required for adaptive responses as well as a key regulator of hypertrophy and hypertrophy-associated genes in the heart. As a leading cause of chronic heart failure, reversal of post-infarction left ventricular remodeling represents an important target for therapeutic interventions. Here we studied the role of GATA-4 as a mediator of post-infarction remodeling. Rats were subjected to experimental myocardial infarction (MI) by ligating the left anterior descending coronary artery (LAD). Ligation of the LAD decreased the DNA binding activity of GATA-4 by 69 % at day 1 after MI (P<0.001, n=7– 8) as assessed by gel mobility shift assays. At 2 weeks the GATA-4 DNA binding was significantly upregulated (2.4-fold, P<0.05, n=7), and returned to baseline at 4 weeks. To determine the functional role of GATA-4, rats underwent LAD ligation followed by peri-infarct intramyocardial delivery of adenoviral vector expressing GATA-4. Hearts treated with the GATA-4 gene transfer exhibited significantly increased ejection fraction (58±5% vs. 38±3% in LacZ-treated control animals with MI, P<0.001, n=8 –9) and fractional shortening (28±3% vs. 16±1%, P<0.001, n=8 –9) 2 weeks after MI. Accordingly, the infarct size was significantly reduced (26±4% vs. 45±4%, P<0.01, n=8 –9). To determine the cardioprotective mechanisms of GATA-4, the number of cardiac stem cells, apoptotic cardiomyocytes and capillaries were assessed. The number of capillaries (59±4/field vs. 48±3/field, P<0.051, n=7– 8) and c-kit positive stem cells (13±5 cells vs. 4±2 cells, P<0.05, n=7– 8) were increased in GATA-4 treated hearts, and a tendency to decreased apoptosis was observed in TUNEL-stained histological sections. These results indicate that the reversal of reduced GATA-4 activity prevents adverse post-infarction remodeling through increased angiogenesis, recruitment of cardiac stem cells and anti-apoptosis. GATA-4-based gene transfer may represent a novel, efficient therapeutic approach for heart failure.

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