Abstract
THE EFFECT OF INTERLEUKIN-6, MICRORNA-21 AND THE ROLE OF ATORVASTATIN IN DILATED CARDIOMYOPATHY- A REVIEW OF LITERATURE

Henry A. Mayala*, Mark Mayala, Reuben Mutta, Khamis Hassan Bakari and Prof. Wang Zhao Hui

ABSTRACT

Myocardial pathologies are major causes of morbidity and mortality worldwide. Ischemic and non-ischemic cardiomyopathies have become a worldwide epidemic of the 21st century with increasing impact on health care systems. Cardiomyopathy is defined as an alteration in the structure and function of the myocardium, leading to deterioration of myocardial performance often resulting in the development of clinical heart failure. Dilated Cardiomyopathy, is a common form of Cardiomyopathy leading to heart failure, has a prevalence of 1:2500 and is characterized by enlargement of one or both of the ventricles with associated systolic dysfunction, microscopically, cardiomyocytes in dilated Cardiomyopathy often consist of a classic histological triad namely; myocyte loss, myocyte hypertrophy and interstitial fibrosis. MicroRNAs are short, non coding RNAs that regulate gene expression at the post-transcriptional level by inhibiting translation or promoting the degradation of target mRNA. Cardiotrophin-1 (CT-1) is a cytokine and a member of the IL-6 family of cytokines. CT-1 mediates its effects by interacting with the glycoprotein 130 (gp130)/leukaemia inhibitory factor receptor beta heterodimer. Statins have lipid lowering and anti-atherosclerotic effects and in addition also have important pleiotropic properties. They limit signal transmission from membrane receptors and slow down pathologic remodelling of the heart and vessels, inhibit the action of angiotensin II, inhibit apoptosis, improve endothelial function, retard the progression of heart failure symptoms, reduce the level of NT-proBNP, restore autonomic nervous system balance and might have a protective influence on renal function and blood pressure.

Keywords: Interleukin-6(IL-6), MicroRNA-21, Atorvastatin, Chronic heart failure (CHF), Cardiac Fibroblasts, Dilated Cardiomyopathy.


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