scholarly journals BYD Ameliorates Oxidative Stress-Induced Myocardial Apoptosis in Heart Failure Post-Acute Myocardial Infarction via the P38 MAPK-CRYAB Signaling Pathway

2018 ◽  
Vol 9 ◽  
Author(s):  
Yi Zhang ◽  
Chun Li ◽  
Hui Meng ◽  
Dongqing Guo ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Myocardial Apoptosis

scholarly journals MicroRNA-383-5p Regulates Oxidative Stress in Mice with Acute Myocardial Infarction through the AMPK Signaling Pathway via PFKM

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Linlin Gao ◽  
Zhongbao Ruan ◽  
Gecai Chen
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Signaling Pathway ◽  
Target Gene ◽  
Ampk Signaling ◽  
Myocardial Apoptosis ◽  
Myocardial Oxidative Stress ◽  
Systolic And Diastolic Function

Objective. The purpose of this study is to explore the regulating role of microRNA-383-5p (miR-383-5p) in oxidative stress after acute myocardial infarction (AMI) through AMPK pathway via phosphofructokinase muscle-type (PFKM). Methods. We established the AMI model, and the model mice were injected with miR-383-5p agomir to study the effect of miR-383-5p in AMPK signaling pathways. The target gene for miR-383-5p was reported to be PFKM, so we hypothesized that overexpression of miR-383-5p inhibits activation of the AMPK signaling pathway. Results. In this research, we found that overexpression of miR-383-5p decreases myocardial oxidative stress, myocardial apoptosis, the expression level of PFKM malondialdehyde (MDA), and reactive oxygen species (ROS) in the myocardial tissues after AMI, and finally, AMI-induced cardiac systolic and diastolic function could be improved.Conclusion. This study demonstrated that miR-383-5p could reduce the oxidative stress after AMI through AMPK signaling pathway by targeting PFKM.

Oxidative stress and hemorheology in patients myocardial infarction with type 2 diabetes

2015 ◽  
Vol 9 (4) ◽  
pp. 0-0 ◽  
Author(s):  
Гончарова ◽  
E. Goncharova ◽  
Ойноткинова ◽  
O. Oynotkinova ◽  
Корниенко ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Lipid Peroxidation ◽  
Acute Heart Failure ◽  
Blood Cells ◽  
Diabetes Type 2 ◽  
Diabetes Type

This paper highlights the influence of the intensity of the oxidative stress on hemorheology parameters in complicated and uncomplicated acute myocardial infarction in patients with diabetes type 2. The study was performed by analyzing the results of examination and treatment of 66 patients, men aged 65,6 ± 5,8 years old, suffering from coronary heart disease with clinical manifestations of acute myocardial infarction and concomitant diabetes type 2. Depending on the presence of acute heart failure patients were divided into 2 groups. 1st group consisted of 34 patients with myocardial infarction without complications, Group 2 - 32 patients who have myocardial infarction complicated by acute heart failure (II-III class classification T.Killip). Condition pro- and antioxidant systems were evaluated for 3 days by determining in the blood of patients diene conjugates, malonic dialdehyde, α-tocopherol, ceruloplasmin, calculated coefficient of oxidative stress. The rheological properties blood evaluated by the blood coagulation time, the hematocrit, amount the fibrinogen in the blood, and blood plasma viscosity, red blood cells deformability index, the aggregation of red blood cells and thrombocytes. The values obtained were compared with data from 32 healthy donors. It is revealed that the development of congestive heart failure in acute myocardial infarction in patients with diabetes type 2 is accompanied by activation of lipid peroxidation (LPO) by maintaining a high level of primary lipid peroxidation products. Insufficient activity of antioxidant defense can limit oxidative processes, and leads to their further growth. The damaging effect of lipid peroxidation in the cell membranes is reflected in violation of aggregation and blood viscosity indexes.

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