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REVIEW ARTICLE
Year : 2011  |  Volume : 2  |  Issue : 3  |  Page : 5

Oxidative stress causes cardio myocyte apoptosis: May be the determinant of development of myocardial disarray in diabetes


1 PhD fellow, School of Biomedical Sciences, Charles Sturt University, Australia
2 Department Physiology, University Technology Sydney, NSW, Australia
3 Clinical Pharmacology, School of Biomedical Sciences, Charles Sturt University, Australia
4 Institute of Nutrition and Food science, University of Dhaka, Bangladesh
5 Neuroscience and pharmacology, School of Biomedical Sciences Charles Sturt University, Australia

Correspondence Address:
S P Lasker
School of Biomedical Sciences, Charles Sturt University, Australia

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Source of Support: None, Conflict of Interest: None


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Oxidative stress resulting from enhanced free radical formation or defect in anti-oxidant defence mechanism, implicates in the development of various disorders including impairment of vasodilatation, neuro degeneration, ventricular dysfunction and changes in cardiac muscle cells morphology. Oxidative stress activates renin aldosterone angiotensin system and inflammatory cytokines that induce apoptosis in heart muscles. It also decreases ATP formation that leads to apoptosis in myocyte. As a consequence, the physical force in the heart is increased that may guide to programme cardiac muscle cell death. The net effect of oxidative stress leads to an architectural rearrangement of the myocardium involving side to side slippage called myocyte disarray. Single myocyte cell death allows side by side translocation of cells. However, multiple cells death causes sliding of the myocyte bundle. No work has yet been done to correlate the myocardial cell slippage and oxidative stress in diabetes, in which heart muscles apoptosis are evident. Thus the present review is done to scrutinize if there is any role of oxidative stress on development of myocyte disarray in diabetes.


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