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BioMed Research International
Volume 2015 (2015), Article ID 273936, 9 pages
http://dx.doi.org/10.1155/2015/273936
Research Article

Induction of Ankrd1 in Dilated Cardiomyopathy Correlates with the Heart Failure Progression

1Department of Integrative Pathophysiology, Medical Faculty Mannheim, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany
2Department of Pathology, Forensic Medicine and Pharmacology, Faculty of Medicine, Vilnius University, M. K. Ciurlionio g. 21, LT-03101 Vilnius, Lithuania
3Vilnius University Hospital Santariskiu Klinikos, Santariškiu g. 2, LT-08661 Vilnius, Lithuania
4State Research Institute, Center for Innovative Medicine, Department of Stem Cell Biology, Žygimantu g. 9, LT-01102 Vilnius, Lithuania
5Vilnius University Institute of Biochemistry, Mokslininku g. 12, LT-08660 Vilnius, Lithuania
6Experimental and Clinical Research Center (ECRC), Max-Delbrueck Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, Buch, 13125 Berlin, Germany

Received 19 August 2014; Accepted 8 October 2014

Academic Editor: Olga Mayans

Copyright © 2015 Julius Bogomolovas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Progression of idiopathic dilated cardiomyopathy (IDCM) is marked with extensive left ventricular remodeling whose clinical manifestations and molecular basis are poorly understood. We aimed to evaluate the clinical potential of titin ligands in monitoring progression of cardiac remodeling associated with end-stage IDCM. Expression patterns of 8 mechanoptotic machinery-associated titin ligands (ANKRD1, ANKRD2, TRIM63, TRIM55, NBR1, MLP, FHL2, and TCAP) were quantitated in endomyocardial biopsies from 25 patients with advanced IDCM. When comparing NYHA disease stages, elevated ANKRD1 expression levels marked transition from NYHA < IV to NYHA IV. ANKRD1 expression levels closely correlated with systolic strain depression and short E wave deceleration time, as determined by echocardiography. On molecular level, myocardial ANKRD1 and serum adiponectin correlated with low BAX/BCL-2 ratios, indicative of antiapoptotic tissue propensity observed during the worsening of heart failure. ANKRD1 is a potential marker for cardiac remodeling and disease progression in IDCM. ANKRD1 expression correlated with reduced cardiac contractility and compliance. The association of ANKRD1 with antiapoptotic response suggests its role as myocyte survival factor during late stage heart disease, warranting further studies on ANKRD1 during end-stage heart failure.