scholarly journals Common matrix metalloproteinase 2 gene haplotypes may modulate left ventricular remodelling in hypertensive patients

2011 ◽  
Vol 26 (3) ◽  
pp. 171-177 ◽  
Author(s):  
R Lacchini ◽  
A L B Jacob-Ferreira ◽  
M R Luizon ◽  
S Gasparini ◽  
M C S Ferreira-Sae ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling ◽  
Hypertensive Patients

scholarly journals Effect of rosuvastatin and benazepril on matrix metalloproteinase-2, matrix metalloproteinase-9 and leukotriene B4 of patients with acute myocardial infarction

2021 ◽  
Vol 18 (3) ◽  
pp. 625-630
Author(s):  
Li Sai ◽  
Zhang YanQiu ◽  
Cui DongMei ◽  
Li YinJun
Keyword(s):  
Matrix Metalloproteinase ◽  
Cardiovascular Events ◽  
Serum Levels ◽  
Leukotriene B4 ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Control Group ◽  
Study Group ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling

Purpose: To investigate the effects of rosuvastatin and benazepril on matrix metalloproteinase-2 (MMP-2), MMP-9 and leukotriene B4 (LTB4) of patients with acute myocardial infarction (AMI). Methods: Fifty-six patients with AMI were selected. They were randomly divided into control and study groups. Thirty healthy people were used in the normal group. On the basis of conventional therapy, patients in the control group were given rosuvastatin orally, while those in the study group received rosuvastatin and benazepril orally. The duration of treatment in both groups was 3 months. Serum levels of MMP-2, MMP-9 and LTB4, and incidence of left ventricular remodelling and recurrence of cardiovascular events were determined before and after treatment for both groups. Results: MMP-2, MMP-9 and LTB4 levels in serum were significantly lower for the two groups after treatment, when compared to pre-treatment values, and significantly lower in the study group (p < 0.05). Left ventricular remodelling was lower in the study group than in the control group (p < 0.05). Recurrence of cardiovascular events declined significantly in the study group, relative to control (p > 0.05). Conclusion: Rosuvastatin and benazepril significantly reduce serum levels of MMP-2, MMP-9 and LTB4 in AMI patients, and thus can potentially prevent ventricular remodelling, improve prognosis and reduce recurrence rate.

scholarly journals MMP inhibitors attenuate doxorubicin cardiotoxicity by preventing intracellular and extracellular matrix remodelling

2020 ◽  
Author(s):  
Brandon Y H Chan ◽  
Andrej Roczkowsky ◽  
Woo Jung Cho ◽  
Mathieu Poirier ◽  
Consolato Sergi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Embryonic Stem ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Left Ventricular Ejection ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling ◽  
Ventricular Ejection Fraction ◽  
Mmp Inhibitors ◽  
Extracellular Matrix Remodelling

Abstract Aims Heart failure is a major complication in cancer treatment due to the cardiotoxic effects of anticancer drugs, especially from the anthracyclines such as doxorubicin (DXR). DXR enhances oxidative stress and stimulates matrix metalloproteinase-2 (MMP-2) in cardiomyocytes. We investigated whether MMP inhibitors protect against DXR cardiotoxicity given the role of MMP-2 in proteolyzing sarcomeric proteins in the heart and remodelling the extracellular matrix. Methods and results Eight-week-old male C57BL/6J mice were treated with DXR weekly with or without MMP inhibitors doxycycline or ONO-4817 by daily oral gavage for 4 weeks. Echocardiography was used to determine cardiac function and left ventricular remodelling before and after treatment. MMP inhibitors ameliorated DXR-induced systolic and diastolic dysfunction by reducing the loss in left ventricular ejection fraction, fractional shortening, and E′/A′. MMP inhibitors attenuated adverse left ventricular remodelling, reduced cardiomyocyte dropout, and prevented myocardial fibrosis. DXR increased myocardial MMP-2 activity in part also by upregulating N-terminal truncated MMP-2. Immunogold transmission electron microscopy showed that DXR elevated MMP-2 levels within the sarcomere and mitochondria which were associated with myofilament lysis, mitochondrial degeneration, and T-tubule distention. DXR-induced myofilament lysis was associated with increased titin proteolysis in the heart which was prevented by ONO-4817. DXR also increased the level and activity of MMP-2 in human embryonic stem cell-derived cardiomyocytes, which was reduced by ONO-4817. Conclusions MMP-2 activation is an early event in DXR cardiotoxicity and contributes to myofilament lysis by proteolyzing cardiac titin. Two orally available MMP inhibitors ameliorated DXR cardiotoxicity by attenuating intracellular and extracellular matrix remodelling, suggesting their use may be a potential prophylactic strategy to prevent heart injury during chemotherapy.

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