scholarly journals The role of Green Tea in experimental myocardial infarction

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Beatriz Lustosa ◽  
Diego Batista ◽  
Bertha Polegato ◽  
Marcos Minicucci ◽  
Elenize Pereira ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Green Tea ◽  
Experimental Myocardial Infarction

Role of delayed intraaortic balloon pumping in treatment of experimental myocardial infarction

1978 ◽  
Vol 41 (7) ◽  
pp. 1202-1208 ◽  
Author(s):  
Arthur J. Roberts ◽  
Daniel R. Alonso ◽  
John R. Combes ◽  
Jerome G. Jacobstein ◽  
Martin R. Post ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Experimental Myocardial Infarction ◽  
Intraaortic Balloon ◽  
Intraaortic Balloon Pumping

scholarly journals Cardioprotective Role of SIRT5 in Response to Acute Ischemia Through a Novel Liver-Cardiac Crosstalk Mechanism

2021 ◽  
Vol 9 ◽  
Author(s):  
Boda Zhou ◽  
Min Xiao ◽  
Hao Hu ◽  
Xiaoxia Pei ◽  
Yajun Xue ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Fibrosis ◽  
Posttranslational Modifications ◽  
Tricarboxylic Acid Cycle ◽  
Liver Mitochondria ◽  
Experimental Myocardial Infarction ◽  
Fibroblast Growth Factor 21 ◽  
Acute Ischemia ◽  
Mice Liver

Protein posttranslational modifications play important roles in cardiovascular diseases. The authors’ previous report showed that the abundance of succinylated and glutarylated proteins was significantly lower in the serum of patients with acute myocardial infarction (AMI) than in that of healthy volunteers, suggesting a potential relationship between protein acylation and AMI. Sirtuin 5 (SIRT5) facilitates the removal of malonyl, succinyl, and glutaryl modification; however, its effects on AMI remain unknown. In this study, the levels of SIRT5 in AMI mouse model was compared. Results showed elevated hepatic SIRT5 after myocardial infarction. Hepatocyte-specific SIRT5 overexpressing mice (liver SIRT5 OE) were generated to address the possible involvement of hepatic SIRT5 in AMI. The areas of myocardial infarction, myocardial fibrosis, and cardiac function in a model of experimental myocardial infarction were compared between liver SIRT5 OE mice and wild-type (WT) mice. The liver SIRT5 OE mice showed a significantly smaller area of myocardial infarction and myocardial fibrosis than the WT mice. The fibroblast growth factor 21 (FGF21) in the blood and myocardium of liver SIRT5 OE mice after AMI was markedly elevated compared with that in WT mice. The results of mass spectrometry showed increased levels of proteins regulating tricarboxylic acid cycle, oxidative phosphorylation, and fatty acid β-oxidation pathways in the liver mitochondria of liver SIRT5 OE mice. These findings showed that SIRT5 may exhibit a cardioprotective effect in response to acute ischemia through a liver-cardiac crosstalk mechanism, probably by increasing the secretion of FGF21 and the improvement of energy metabolism.

Protective Role of ADAMTS13 for Myocardium in Mouse Model of Experimental Myocardial Infarction.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2175-2175
Author(s):  
Masaaki Doi ◽  
Hideto Matsui ◽  
Yukiji Takeda ◽  
Yoshihiko Saito ◽  
Maiko Takeda ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Stroke ◽  
Mouse Model ◽  
Protective Role ◽  
Experimental Myocardial Infarction ◽  
Thrombotic Occlusion ◽  
Cardiac Functions ◽  
Functional Regulation ◽  
Brain Ischemic Stroke

Abstract Abstract 2175 The metalloprotease ADAMTS13 regulates the size of von Willebrand factor (VWF) multimers, controlling excessive VWF functions and preventing thrombotic occlusion of microvasculature. We previously reported that ADAMTS13 deficiency aggravated the extent of brain ischemic stroke in a mouse model of middle cerebral arterial occlusion, suggesting the relevant role of ADAMTS13 in the pathophysiology of brain stroke (Fujioka, et al. Blood, 2010; 115: 1650). These results raised the possibility that the functional regulation of VWF by ADAMTS13 could also play a role in coronary ischemic events such as myocardial infarction. To address this issue, we have used a mouse model of experimental myocardial infarction. The left anterior descending coronary artery in mice was ligated at 2 mm downstream from the origin under thoracotomy with ventilator-assisted respiration, and the cardiac function was evaluated with M-mode echocardiography after 7 days of operation. We compared 20 wild-type (WT) mice and 20 Adamts13 −/− (KO) mice, all of which were 12–14 weeks of age, healthy and fertile. Significantly (p < 0.01) decreased ejection fraction (EF; 44.0±6.7%) and increased left ventricular end-diastolic diameter (LVDd; 4.68±0.69 mm) of KO mice, as compared to WT (EF; 62.7±13.0% and LVDd; 3.77±0.56 mm, respectively), revealed that cardiac functions were apparently more impaired in KO mice. In addition, these reduced cardiac functions observed in KO mice were improved to an extent comparable to those of WT mice by the bolus injection of recombinant human ADAMTS13 (rhADAM; 3 μg/mouse, n=20) just after the operation (KO mice + rhADAM, EF; 58.2.±9.9% and LVDd; 3.16±0.52 mm). Consistent with echocardiography data, histological studies demonstrated the significantly (p < 0.01) higher infarct ratio in myocardium of KO mice (WT; 37.3±18.4%, KO; 59.1±16.3%, KO + rhADAM; 33.7±24.4%). Our results indicate that ADAMTS13, as seen in the case of brain ischemic stroke, plays a protective role for myocardium in coronary artery ischemia, improving myocardial functions and the severity of heart failure. Proper functional regulation of VWF-dependent thrombotic or inflammatory responses by ADAMTS13 could reduce thrombotic occlusion of microvasculature including leukocyte plugging, contributing to better local microcirculation which is crucial for tissue or organ functions. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Double-Edged Role of the CXCL12/CXCR4 Axis in Experimental Myocardial Infarction

2011 ◽  
Vol 58 (23) ◽  
pp. 2415-2423 ◽  
Author(s):  
Elisa A. Liehn ◽  
Nancy Tuchscheerer ◽  
Isabella Kanzler ◽  
Maik Drechsler ◽  
Line Fraemohs ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Experimental Myocardial Infarction ◽  
Cxcr4 Axis

Role of interleukin‐6 for left ventricular remodeling and survival after experimental myocardial infarction

2003 ◽  
Vol 17 (14) ◽  
pp. 1-20 ◽  
Author(s):  
Martin Fuchs ◽  
Andres Hilfiker ◽  
Karol Kaminski ◽  
Denise Hilfiker-Kleiner ◽  
Zeynep Guener ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Interleukin 6 ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction

scholarly journals TNF-Like Weak Inducer of Apoptosis Aggravates Left Ventricular Dysfunction after Myocardial Infarction in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Kai-Uwe Jarr ◽  
Sabine Eschricht ◽  
Linda C. Burkly ◽  
Michael Preusch ◽  
Hugo A. Katus ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Ventricular Dysfunction ◽  
Myocardial Function ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Metabolic Adaptations

Background. TNF-like weak inducer of apoptosis (TWEAK) has recently been shown to be potentially involved in adverse cardiac remodeling. However, neither the exact role of TWEAK itself nor of its receptor Fn14 in this setting is known.Aim of the Study. To analyze the effects of sTWEAK on myocardial function and gene expression in response to experimental myocardial infarction in mice.Results. TWEAK directly suppressed the expression of PGC-1αand genes of oxidative phosphorylation (OXPHOS) in cardiomyocytes. Systemic sTWEAK application after MI resulted in reduced left ventricular function and increased mortality without changes in interstitial fibrosis or infarct size. Molecular analysis revealed decreased phosphorylation of PI3K/Akt and ERK1/2 pathways associated with reduced expression of PGC-1αand PPARα. Likewise, expression of OXPHOS genes such as atp5O, cycs, cox5b, and ndufb5 was also reduced. Fn14-/-mice showed significantly improved left ventricular function and PGC-1αlevels after MI compared to their respective WT littermates (Fn14 +/+). Finally, inhibition of intrinsic TWEAK with anti-TWEAK antibodies resulted in improved left ventricular function and survival.Conclusions. TWEAK exerted maladaptive effects in mice after myocardial infarction most likely via direct effects on cardiomyocytes. Analysis of the potential mechanisms revealed that TWEAK reduced metabolic adaptations to increased cardiac workload by inhibition of PGC-1α.

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