scholarly journals Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction

2000 ◽  
Vol 106 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Anique Ducharme ◽  
Stefan Frantz ◽  
Masanori Aikawa ◽  
Elena Rabkin ◽  
Merry Lindsey ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Matrix Metalloproteinase 9 ◽  
Ventricular Enlargement ◽  
Targeted Deletion ◽  
Collagen Accumulation ◽  
Metalloproteinase 9 ◽  
Left Ventricular Enlargement

scholarly journals Matrix Metalloproteinase Inhibition Attenuates Early Left Ventricular Enlargement After Experimental Myocardial Infarction in Mice

Circulation ◽  
1999 ◽  
Vol 99 (23) ◽  
pp. 3063-3070 ◽  
Author(s):  
Luis E. Rohde ◽  
Anique Ducharme ◽  
Luis H. Arroyo ◽  
Masanori Aikawa ◽  
Galina H. Sukhova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Ventricular Enlargement ◽  
Left Ventricular Enlargement

scholarly journals Macrophage overexpression of matrix metalloproteinase-9 in aged mice improves diastolic physiology and cardiac wound healing after myocardial infarction

2018 ◽  
Vol 314 (2) ◽  
pp. H224-H235 ◽  
Author(s):  
Cesar A. Meschiari ◽  
Mira Jung ◽  
Rugmani Padmanabhan Iyer ◽  
Andriy Yabluchanskiy ◽  
Hiroe Toba ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Wound Healing ◽  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Transforming Growth Factor ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 9 ◽  
Sequencing Analysis ◽  
Metalloproteinase 9 ◽  
Cardiac Wound Healing

Matrix metalloproteinase (MMP)-9 increases in the myocardium with advanced age and after myocardial infarction (MI). Because young transgenic (TG) mice overexpressing human MMP-9 only in macrophages show better outcomes post-MI, whereas aged TG mice show a worse aging phenotype, we wanted to evaluate the effect of aging superimposed on MI to see if the detrimental effect of aging counteracted the benefits of macrophage MMP-9 overexpression. We used 17- to 28-mo-old male and female C57BL/6J wild-type (WT) and TG mice ( n = 10–21 mice/group) to evaluate the effects of aging superimposed on MI. Despite similar infarct areas and mortality rates at day 7 post-MI, aging TG mice showed improved diastolic properties and remodeling index compared with WT mice (both P < 0.05). Macrophage numbers were higher in TG than WT mice at days 0 and 7 post-MI, and the post-MI increase was due to elevated cluster of differentiation 18 protein levels (all P < 0.05). RNA sequencing analysis of cardiac macrophages isolated from day 7 post-MI infarcts identified 1,276 statistically different (all P < 0.05) genes (994 increased and 282 decreased in TG mice). Reduced expression of vascular endothelial growth factor A, platelet-derived growth factor subunit A, and transforming growth factor-β3, along with elevated expression of tissue inhibitor of MMP-4, in macrophages revealed mechanisms of indirect downstream effects on fibroblasts and neovascularization. While collagen accumulation was enhanced in TG mice compared with WT mice at days 0 and 7 post-MI ( P < 0.05 for both), the post-MI collagen cross-linking ratio was higher in WT mice ( P < 0.05), consistent with increased diastolic volumes. Vessel numbers [by Griffonia ( Bandeiraea) simplicifolia lectin I staining] were decreased in TG mice compared with WT mice at days 0 and 7 post-MI ( P < 0.05 for both). In conclusion, macrophage-derived MMP-9 improved post-MI cardiac wound healing through direct and indirect mechanisms to improve diastolic physiology and remodeling.NEW & NOTEWORTHY Aging mice with macrophage overexpression of matrix metalloproteinase-9 have increased macrophage numbers 7 days after myocardial infarction, resulting in improved diastolic physiology and left ventricular remodeling through effects on cardiac wound healing.

scholarly journals Effects of Quercetin on Cardiac Fibrosis in Patients with Acute Myocardial Infarction and Arterial Hypertension

2017 ◽  
Vol 24 (2) ◽  
Author(s):  
Wael Rumaneh ◽  
Iryna Kupnovytska
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Arterial Hypertension ◽  
Plasma Levels ◽  
Cardiac Fibrosis ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 9 ◽  
Pharmacological Management ◽  
Metalloproteinase 9

Arterial hypertension is an independent predictor of acute myocardial infarction. Nowadays, plasma levels of fibronectin and matrix metalloproteinase 9 are the markers of left ventricular remodeling.The objective of the research was to investigate potential antifibrotic effects of Quercetin in patients with acute myocardial infarction and arterial hypertension.Material and methods. 130 patients with myocardial infarction (63 individuals with concomitant arterial hypertension and 67 individuals without it) were observed. All the patients were divided into groups of basic treatment and additional prescription of Quercetin. Transthoracic echocardiogram was used. To evaluate plasma level of fibronectin and matrix metalloproteinase 9 the ELISA method was applied.Results. In all the patients, a significant decrease in fibronectin plasma levels was observed since the 28th day of treatment; however, it was more significant in group of additional prescription of Quercetin. Revascularization and pharmacological management of myocardial infarction resulted in the reduction in matrix metalloproteinase 9 plasma levels in all the patients since the 7th day of treatment; however, it was more significant in group of additional prescription of Quercetin. Conclusions. Quercetin possesses potential antifibrotic properties causing a reduction in plasma levels of fibronectin and matrix metalloproteinase 9 in patients with myocardial infarction and concomitant arterial hypertension.

Sign in / Sign up

Export Citation Format

Share Document