Balkan Journal of Medical Genetics

INCREASED EXPRESSION OF CARDIOTROPHIN-1 IN CARDIOMYOPATHY PATIENTS
Sharif S1,*, Saleem A1, Naz S1, Rashid F1, Iqtedar M2, Kaleem A2, Latif A1
*Corresponding Author: Dr. Saima Sharif, Department of Zoology, Lahore College for Women University, Jail Road, Lahore, Pakistan. Tel: +92-333-409-2232. Fax: +92-042-9920-3077. E-mail: saimasharif04@ gmail.com
page: 21

INTRODUCTION

Cardiomyopathy (CM) is a progressive disease of the myocardium or heart muscle, resulting in heart failure [1]. Heart muscle disorders occur due to a heterogeneous group of CM. In the absence of abnormal loading conditions or ischemic heart disease, abnormal myocardial structure and function is present in CM [2]. In the autosomal dominant forms of CM incomplete expression is common. On the basis of morphology and function, CM is classified into four groups: dilated CM (DCM), hypertrophic CM (HCM), restrictive CM (RCM) and arrhythmogenic right ventricular (RV) CM/dysplasia (ARVC/D) [2]. Worldwide, the most widespread CM is DCM. Dilated CM is a disorder in heart muscles, in which left or both ventricles become dilated and perform poor function [3]. More than 1400 mutations are associated with CM. Most of these mutations are located on genes encoding the proteins of thick and thin sarcomere filaments. Small numbers of mutations have been observed in genes which encode Z-disc components and handle calcium proteins [4]. The most common causes of CM are viral infection, alcohol, family history, age, sex, hyperglycemia, diabetes mellitus, abnormal thyroid function and heart attack. Symptoms of heart failure (HF) may include shortness of breath, fatigue, cough, orthopnea, paroxysmal nocturnal dyspnea, and edema [5,6]. Some physical activities (vigorous, moderate and sedentary life style) and etiological attributes may contribute in this disease [7]. Cardiotrophin-1 (CT-1) is an interleukin-6 (IL-6) family cytokine and is an active inducer capable of cardiac hypertrophy and vascular stiffness in hypertensive heart disease [8]. It is capable of recapitulating the physiological growth of the heart including transient and reversible hypertrophy of the myocardium [9]. In the human aortic vascular smooth muscle cells, CT-1 stimulate the proliferation migration and collagen-1 (COL1) expression. In vascular endothelial cells and monocyte migration, proatherogenic expression is stimulated by CT-1. Atherosclerotic lesions formed by formation of foam cells and COL1 production [10]. The purpose of present study was to examine the expression of CT-1 in CM in the local population.

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