GW29-e1773 Enhanced oxidative stress mediates pathological autophagy in cardiac myocytes in pressure overload induced heart failure in rats

The Role of Oxidative Stress and Antioxidants in Occurrence of Myocardial Infarction and Chronic Heart Failure

“…The function of mitochondria is to sustain numerous homeostatic processes in the heart, including generation of energy and control of calcium metabolism and redox homeostasis [1]. The majority of free radicals in cardiomyocytes is produced in mitochondria and by nicotinamide adenine dinucleotide phosphate oxidase, Oxidative stress and myocyte autophagy coexist in pressure overload-induced heart failure [9]. Oxidative capacity of the cardiac muscle, mitochondrial content, and mitochondrial fusion are abnormal in elderly patients with heart failure with preserved ejection fraction and could contribute to physical load intolerance in such patients [10].…”

“…The benefi cial effects of malonyl coenzyme A decarboxylase inhibition were attributed to a decrease in proton production due to an improved coupling between glycolysis and glucose oxidation in rats during experimental myocardial infarction [12]. All lipoproteins, proteins and nucleic acids are targets for free radical activity, which leading to their oxidative modifi cation [1,3,9]. Proteins with modifi ed amino acid residues are involved in the pathogenesis of metabolic and structural disorders in various diseases [13].…”

“…Cell senescence characterised by mitotic arrest and stimuli generation of the great number of proinfl ammatory and growth factors, leading to an increase of tissue infl ammation and oxidative stress [1]. Generation of oxidative stress mediates pathological autophagy in cardiomyocytes leading to left ventricle dysfunction and antioxidants are capable of preventing pressure overload-induced heart failure through inhibition of excessive cardiomyocyte apoptosis [9]. The content of lipoperoxides glows gradually from the moment of myo cardial infarction occurrence over a period of 21 days.…”

“…During progressive angina pectoris without development of MI, the concentration of serum iron also exceeds normal values, but does not reach the level that is observed in case of myocardial infarction [53]. Anaemia is in correlation with premature development of coronary heart disease, chronic heart failure, cardiac arrhythmias and sudden death from cardiac pathology [1,9]. Concentrations of pro-infl ammatory markers of interleukin-6, interleukin-10 and C-reactive protein in patients with myocardial infarction, along with the value of ferritin, correlate with the risk of sudden death in patients with coronary artery disease [40,54,55].…”